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	<updated>2026-08-19T22:32:10Z</updated>
	<subtitle>User contributions</subtitle>
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	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_citation&amp;diff=7190</id>
		<title>Satellite citation</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_citation&amp;diff=7190"/>
		<updated>2014-02-24T14:08:13Z</updated>

		<summary type="html">&lt;p&gt;Yulia: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;* Jessica Severin,  Marina Lizio, Jayson Harshbarger, Hideya Kawaji, Carsten O Daub, Yoshihide Hayashizaki, the FANTOM consortium, Nicolas Bertin, and Alistair RR Forrest. “Interactive visualization and analysis of large-scale NGS data-sets using ZENBU”. Nature Biotechnology, http://dx.doi.org/10.1038/nbt.2840 (2013)&lt;br /&gt;
&lt;br /&gt;
* Hideya Kawaji, Marina Lizio, Masayoshi Itoh, Mutsumi Kanamori-Katayama, Ai Kaiho, Hiromi Nishiyori-Sueki, Jay W. Shin, Miki Kojima-Ishiyama, Mitsuoki Kawano, Mitsuyoshi Murata, Noriko Ninomiya-Fukuda, Sachi Ishikawa-Kato, Sayaka Nagao-Sato, Shohei Noma, Yoshihide Hayashizaki, Alistair R.R. Forrest, Piero Carninci, and the FANTOM consortium. &amp;quot;Comparison of CAGE and RNA-seq transcriptome profiling using a clonally amplified and single molecule next generation sequencing&amp;quot;. Genome Research, doi: 10.1101/gr.156232.113 &lt;br /&gt;
&lt;br /&gt;
* Robin Andersson, Claudia Gebhard, Irene Miguel-Escalada, Ilka Hoof, Jette Bornholdt, Mette Boyd, Yun Chen, Xiaobei Zhao, Christian Schmidl, Takahiro Suzuki, Evgenia Ntini, Erik Arner,, Eivind Valen,, Kang Li, Lucia Schwarzfischer, Dagmar Glatz, Johanna Raithel, Berit Lilje, Nicolas Rapin,, Frederik Otzen Bagger,, Mette Jørgensen, Peter Refsing Andersen, Nicolas Bertin,, Owen Rackham,, A. Maxwell Burroughs,, J. Kenneth Baillie, Yuri Ishizu,, Yuri Shimizu, Erina Furuhata, Shiori Maeda,, Yutaka Negishi,, Christopher J. Mungall, Terrence F. Meehan, Timo Lassmann, Masayoshi Itoh,,, Hideya Kawaji,, Naoto Kondo,, Jun Kawai,, Andreas Lennartsson, Carsten O. Daub,Peter Heutink, David A. Hume, Torben Heick Jensen, Harukazu Suzuki, Yoshihide Hayashizaki, Ferenc Müller, the FANTOM consortium,  Alistair R.R. Forrest Piero Carninci Michael Rehli Albin Sandelin. &amp;quot;An atlas of active enhancers across human cell types and tissues&amp;quot; Nature doi:10.1038/nature12787&lt;br /&gt;
&lt;br /&gt;
* Yulia A Medvedeva, Abdullah M Khamis, Ivan V Kulakovskiy, Wail Ba-Alawi, Md Shariful I Bhuyan, Hideya Kawaji, Timo Lassmann, Matthias Harbers, Alistair RR Forrest, Vladimir B Bajic and The FANTOM consortium, BMC Genomics 2013,15:119 doi:10.1186/1471-2164-15-119&lt;br /&gt;
&lt;br /&gt;
* Regarding to the public version of &amp;quot;resource browser&amp;quot;, please refer it as SSTAR ( http://fantom.gsc.riken.jp/5/sstar/ )&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_citation&amp;diff=7189</id>
		<title>Satellite citation</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_citation&amp;diff=7189"/>
		<updated>2014-02-24T14:06:54Z</updated>

		<summary type="html">&lt;p&gt;Yulia: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;* Jessica Severin,  Marina Lizio, Jayson Harshbarger, Hideya Kawaji, Carsten O Daub, Yoshihide Hayashizaki, the FANTOM consortium, Nicolas Bertin, and Alistair RR Forrest. “Interactive visualization and analysis of large-scale NGS data-sets using ZENBU”. Nature Biotechnology, http://dx.doi.org/10.1038/nbt.2840 (2013)&lt;br /&gt;
&lt;br /&gt;
* Hideya Kawaji, Marina Lizio, Masayoshi Itoh, Mutsumi Kanamori-Katayama, Ai Kaiho, Hiromi Nishiyori-Sueki, Jay W. Shin, Miki Kojima-Ishiyama, Mitsuoki Kawano, Mitsuyoshi Murata, Noriko Ninomiya-Fukuda, Sachi Ishikawa-Kato, Sayaka Nagao-Sato, Shohei Noma, Yoshihide Hayashizaki, Alistair R.R. Forrest, Piero Carninci, and the FANTOM consortium. &amp;quot;Comparison of CAGE and RNA-seq transcriptome profiling using a clonally amplified and single molecule next generation sequencing&amp;quot;. Genome Research, doi: 10.1101/gr.156232.113 &lt;br /&gt;
&lt;br /&gt;
* Robin Andersson, Claudia Gebhard, Irene Miguel-Escalada, Ilka Hoof, Jette Bornholdt, Mette Boyd, Yun Chen, Xiaobei Zhao, Christian Schmidl, Takahiro Suzuki, Evgenia Ntini, Erik Arner,, Eivind Valen,, Kang Li, Lucia Schwarzfischer, Dagmar Glatz, Johanna Raithel, Berit Lilje, Nicolas Rapin,, Frederik Otzen Bagger,, Mette Jørgensen, Peter Refsing Andersen, Nicolas Bertin,, Owen Rackham,, A. Maxwell Burroughs,, J. Kenneth Baillie, Yuri Ishizu,, Yuri Shimizu, Erina Furuhata, Shiori Maeda,, Yutaka Negishi,, Christopher J. Mungall, Terrence F. Meehan, Timo Lassmann, Masayoshi Itoh,,, Hideya Kawaji,, Naoto Kondo,, Jun Kawai,, Andreas Lennartsson, Carsten O. Daub,Peter Heutink, David A. Hume, Torben Heick Jensen, Harukazu Suzuki, Yoshihide Hayashizaki, Ferenc Müller, the FANTOM consortium,  Alistair R.R. Forrest Piero Carninci Michael Rehli Albin Sandelin. &amp;quot;An atlas of active enhancers across human cell types and tissues&amp;quot; Nature doi:10.1038/nature12787&lt;br /&gt;
&lt;br /&gt;
* Yulia A Medvedeva, Abdullah M Khamis, Ivan V Kulakovskiy, Wail Ba-Alawi, Md Shariful I Bhuyan, Hideya Kawaji, Timo Lassmann, Matthias Harbers, Alistair RR Forrest, Vladimir B Bajic and The FANTOM consortium, BMC Genomics 2013,15:119 &lt;br /&gt;
&lt;br /&gt;
* Regarding to the public version of &amp;quot;resource browser&amp;quot;, please refer it as SSTAR ( http://fantom.gsc.riken.jp/5/sstar/ )&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=File:Medvedeva_et_al_accepted.zip&amp;diff=7094</id>
		<title>File:Medvedeva et al accepted.zip</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=File:Medvedeva_et_al_accepted.zip&amp;diff=7094"/>
		<updated>2013-11-28T11:32:44Z</updated>

		<summary type="html">&lt;p&gt;Yulia: uploaded a new version of &amp;quot;File:Medvedeva et al accepted.zip&amp;quot;&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=File:Effect_of_cytosine_methylation_on_transcription_factor_binding_sites_and_regulation_of_transcription.doc&amp;diff=7093</id>
		<title>File:Effect of cytosine methylation on transcription factor binding sites and regulation of transcription.doc</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=File:Effect_of_cytosine_methylation_on_transcription_factor_binding_sites_and_regulation_of_transcription.doc&amp;diff=7093"/>
		<updated>2013-11-28T11:19:15Z</updated>

		<summary type="html">&lt;p&gt;Yulia: uploaded a new version of &amp;quot;File:Effect of cytosine methylation on transcription factor binding sites and regulation of transcription.doc&amp;quot;&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=File:Medvedeva_et_al_accepted.zip&amp;diff=7056</id>
		<title>File:Medvedeva et al accepted.zip</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=File:Medvedeva_et_al_accepted.zip&amp;diff=7056"/>
		<updated>2013-11-05T12:41:39Z</updated>

		<summary type="html">&lt;p&gt;Yulia: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_submission&amp;diff=7055</id>
		<title>Satellite submission</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_submission&amp;diff=7055"/>
		<updated>2013-11-05T12:38:56Z</updated>

		<summary type="html">&lt;p&gt;Yulia: /* Title: Effect of cytosine methylation on transcription factor binding sites and regulation of transcription */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;== Satellite manuscript internal review page  ==&lt;br /&gt;
&lt;br /&gt;
Welcome to the FANTOM5 Satellite review page. As discussed at the Ume and Koyo meetings, all papers will be visible to consortium members. This is to allow everyone to know what is going on, promote collaboration, carry out due process regarding co-authorship and to avoid competition. &lt;br /&gt;
&lt;br /&gt;
== Authorship  ==&lt;br /&gt;
&lt;br /&gt;
The author list will basically be selected by the first author and the corresponding author of each satellite paper on the basis of the scientific contribution to the manuscript. Remember to include an authors contribution statement for all authors named in your manuscript (of the form AB carried out the cell isolation, SB carried out the network predictions etc.). &lt;br /&gt;
&lt;br /&gt;
In addition the FANTOM5 headquarter will name RIKEN OSC members who should be co-authors for their input on each manuscript and to the entire FANTOM5 project. For those of you who have participated in previous FANTOMs you will be familiar with this process, for those new to FANTOM please look at the author lists on the satellite paper collections for FANTOM2-4. FANTOM5 headquarter is currently discussing the policy for RIKEN OSC co-authorship on the FANTOM5 satellites, but basically satellites papers will be considered on a case by case basis, and will take into account datasets used, intellectual input and facilitating technologies/analyses for each paper. &lt;br /&gt;
&lt;br /&gt;
At this stage please name any authors from the OSC that you think should definitely be included as co-authors, in addition for all satellite submissions include the following term &#039;&#039;&#039;RIKEN_OSC_members&#039;&#039;&#039; as an additional author. &lt;br /&gt;
&lt;br /&gt;
== Instructions  ==&lt;br /&gt;
&lt;br /&gt;
Please make a copy of the template below and enter your manuscript details. &lt;br /&gt;
&lt;br /&gt;
If you are not able to edit the wiki yourself please email the secretariat with the subject line &amp;quot;FANTOM5_satellite&amp;quot;, but please understand that these will be processed when we can rather than immediately. You must fill in all of the details below and provide both a PDF that contains all figures, and word doc of the main text, for reviewers to mark up directly. &lt;br /&gt;
&lt;br /&gt;
== RIKEN affiliation and acknowledgements in Satellite papers - guidelines ==&lt;br /&gt;
&lt;br /&gt;
As of April 1st, 2013, Omics Science Center has ceased to exist as a part of RIKEN reorganization. Many OSC members have changed their affiliation to other RIKEN centers or institutions. Therefore there has been a change in the way affiliations and acknowledgements are written on the Phase 1 satellite papers.&lt;br /&gt;
&lt;br /&gt;
Please consult the below guidelines before submitting the paper. For the existing manuscripts/manuscripts under submission please change affiliations and acknowledgements accordingly.&lt;br /&gt;
&lt;br /&gt;
Also, authors should &#039;&#039;&#039;send the manuscripts to &#039;&#039;&#039;[mailto:fantom5-secretariat@gsc.riken.jp FANTOM5 Secretariat] for checks before submitting the paper or the final proof to avoid trouble later.&lt;br /&gt;
&lt;br /&gt;
Guidelines: [[File: F5_affiliation_acknowledgements_130816.pdf]]&lt;br /&gt;
&lt;br /&gt;
= Manuscripts  =&lt;br /&gt;
&lt;br /&gt;
== Title: Epigenetic factors regulating Hematopoiesis  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_004 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;The hematopoietic differentiation pathway is a complex regulatory program for generating different lineages of blood cell types from multipotent, hematopoietic stem cells. The transcriptional program dictating hematopoietic cell fate and differentiation requires an epigenetic memory function consisting of a network of enzymes controlling DNA methylation, histone posttranslational modifications and chromatin structure. Defective interactions between epigenetic enzymes and transcription factors cause perturbations in blood cell differentiation, which often leads to various types of hematopoietic disorders such as leukemia. To elucidate the contribution of different epigenetic factors in human hematopoieis, high-throughput Cap Analysis of Gene Expression (CAGE) sequencing was used to build comprehensive transcription profiles of 199 epigenetic factors in a wide range of blood cells. These epigenetic factors include proteins that covalently modify DNA/histones or alter chromatin structure dynamics. Our analysis revealed several epigenetic factors to have expression profiles specific for cell type, lineage type and/or leukemic cell lines. In this report the ‘epigenetic transcriptome’ has been systematically studied to predict their potential functions in the epigenetic regulatory network of human hematopoiesis. The potential of such a comprehensive study is not only to identify putative epigenetic regulators of normal hematopoiesis and postulate their function but also to serve as a resource for the scientific community for further characterization and validation of differentially expressed transcripts. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Punit Prasad, Michelle Rönnerblad,...FANTOM5, Erik Arner, Karl Ekwall and Andreas Lennartsson &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;PP and MR have done analysis and written the manuscript. EA has performed the initial CAGE analysis for the epigenetic factors and assisted in writing the manuscript. AL and KE have assisted in writing the manuscript, planned and coordinated the study. The authors declare no conflict of interest.&amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ... &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Blood or other&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;December 06, 2012&amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:andreas.lennartsson@ki.se,arner@gsc.riken.jp Andreas Lennartsson, Erik Arner] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Prasad et al Blood 020213 .docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Prasad et al Blood 020213 .pdf]] &lt;br /&gt;
&lt;br /&gt;
----&lt;br /&gt;
== Title: Redefinition of the human mast cell transcriptome by deep-CAGE sequencing ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_009 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;Despite their haematopoietic origin, mast cells (MCs) mature exclusively in peripheral tissues, hampering research into their developmental and functional programs. Here, we employed deep-CAGE on skin-derived MCs to generate the most comprehensive view of the human MC transcriptome ever reported. A particular advantage is that MCs were embedded in the FANTOM5 project, giving the opportunity to contrast their molecular signature against an extensive panel of human samples. We demonstrate that MCs possess a unique and surprising transcriptional landscape, combining expression of typical haematopoietic genes with those exclusively active in MCs, and genes not previously reported as expressed in MCs. Specifically we found that MCs express functional BMP receptors, which transduce pro-survival and activatory signals. Conversely, several genes frequently studied in MCs were either not or only weakly expressed in direct comparison with other myelocytes. By the parallel use of MCs ex vivo and following culture, we also found that MCs change their transcriptome in in vitro surroundings. Befitting their uniqueness, MCs had no close relative in the haematopoietic network. This rich dataset reveals that our knowledge of human MCs is still fairly limited. It can be anticipated that with this resource novel functional programs of MCs will soon be discovered.&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Efthymios Motakis,1,* Sven Guhl,2,* Yuri Ishizu,1 RIKEN OSC members,1 Torsten Zuberbier,2 Alistair R R Forrest,1¶ Magda Babina2¶&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;E.M. carried out bioifnormatics analayses S.G. isolated the mast cells and performed most experiments, M.B. performed several experiments, was involved in planning, supervision, and data analysis, and wrote the first draft of the manuscript, E.M. S.G., A.R.R.F. and T.Z. helped with planning, data analysis and manuscript writing. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on mast cell samples in comparison to freeze 1 data &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Blood, eBlood &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:magda.babina@charite.de,sven.guhl@charite.de Magda Babina, Sven Guhl] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:BLOOD-2013-483792v1-Forrest.pdf]] &lt;br /&gt;
&lt;br /&gt;
----&lt;br /&gt;
== Title: Transcription and enhancer profiling in human monocyte subsets  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_011 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Human blood monocytes comprise at least three subpopulations that differ in phenotype and function. Here we present the first in-depth regulome analysis of classical (CD14++CD16-), intermediate (CD14+CD16+), and nonclassical (CD14dimCD16+) monocytes. Cap Analysis of Gene Expression (CAGE) adapted to Helicos single molecule sequencing was used to map transcription start sites throughout the genome in all three subsets. In addition, global maps of H3K4me1 and H3K27ac deposition were generated for classical and nonclassical monocytes defining enhanceosomes of the two major subsets. We identify differential regulatory elements (including promoters and putative enhancers) that were associated with subset-specific motif signatures corresponding to different transcription factor activities and exemplarily validate a novel downstream enhancer of the CD14 locus. In addition to known subset specific features, pathway analysis revealed marked differences in metabolic gene signatures. While classical monocytes expressed higher levels of genes involved in carbohydrate metabolism priming them for anaerobic energy production, nonclassical monocytes expressed higher levels of oxidative pathway components and showed a higher routine mitochondrial activity. Our findings describe promoter/enhancer landscapes and provide novel insights into the specific biology of human monocyte subsets. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Christian Schmidl, Kathrin Renner, Ruediger Eder, Katrin Peter, Petra Hoffmann, Reinhard Andreesen, Marina P. Kreutz, RIKEN_OSC_members, Matthias Edinger, Michael Rehli &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;CS performed experiments, computational analyses and wrote parts of the manuscript writing, KR performed experiments and contributed to manuscript writing, RE isolated the cells, KP performed experiments, PH, RA, MK, and ME contributed to planning and supervision, RIKEN_OSC_members who organized or performed Helicos sequencing and provided aligned data; MR initiated, planned and supervised the study, performed computational analyses, and wrote the manuscript. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on monocyte subsets (Regensburg samples) &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Blood, eBlood, other &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: September 1 ,2012 &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:michael.rehli@ukr.de,Christian.Schmidl@klinik.uni-regensburg.de Michael Rehli, Christian Schmidl] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Schmidl MonoSub.docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Schmidl MonoSub.pdf]]&amp;amp;nbsp;&amp;amp;nbsp; &lt;br /&gt;
&lt;br /&gt;
----&lt;br /&gt;
&lt;br /&gt;
== Title:The enhancer and promoter landscape of regulatory and conventional T cell subpopulations  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_34&amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; CD4+CD25+FOXP3+ human regulatory T cells (Treg) are essential for self-tolerance and immune homeostasis. Here, we describe the promoterome of CD4+CD25highCD45RA+ naïve and CD4+CD25highCD45RA– memory Treg and their CD25– conventional T cell (Tconv) counterparts both before and after in vitro expansion by cap analysis of gene expression adapted to single molecule sequencing (HeliscopeCAGE). We performed comprehensive comparative digital gene expression analyses and revealed new orphan transcription start sites, of which several were validated as alternative promoters of known genes including FOXP3 and CTLA4. For all in vitro expanded subsets, we additionally generated genome-wide maps of poised and active enhancer elements marked by histone H3 lysine 4 monomethylation and histone H3 lysine 27 acetylation. Analysis of cell type-specific regulatory elements revealed a specific enrichment of several transcription factor binding motifs. We validated promising candidates by chromatin immunoprecipitation coupled to next generation sequencing and identified STAT5 and FOXP3 as well as RUNX1 and ETS1 as global regulators of Treg- and Tconv-specific enhancers, respectively. In summary we provide a highly detailed and easily accessible resource of gene expression and -regulation in Treg and Tconv subpopulations. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: R&#039;&#039;&#039; &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Blood&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:christian.schmidl@klinik.uni-regensburg.de,michael.rehli@klinik.uni-regensburg.de Christian Schmidl, Michael Rehli] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:121027 FANTOM Treg manuscript.docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Schmidl Treg.pdf]] &lt;br /&gt;
&lt;br /&gt;
----&lt;br /&gt;
&lt;br /&gt;
== Title: Effect of cytosine methylation on transcription factor binding sites and regulation of transcription  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_010 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BMC GENOMICS&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Background: DNA methylation in promoters is strongly linked to downstream gene repression. However, the question remains as to whether DNA methylation is a cause or a consequence of gene repression. In the former case, DNA methylation may affect the affinity of transcription factors (TFs) towards their binding sites (TFBSs). In the latter case, gene repression caused by chromatin modification is stabilized by DNA methylation. Until now, the above-mentioned scenarios have been only supported only by non-systematic evidences and have not been tested for a wide spectrum of TFs. Although the average promoter methylation is usually used in related studies, recent results suggested that methylation of individual cytosines can be also important. &amp;lt;br&amp;gt; Results: We found that for 16.6% of cytosines methylation profile and the expression profile of neighboring TSSs were significantly anti-correlated. We named CpG corresponding to such cytosines as “traffic lights”. We observed a strong selection against CpG “traffic lights” within TFBSs. The negative selection was stronger for transcriptional repressors as compared to transcriptional activators or multifunctional TFs as well as for core TFBS positions as compared to flanking TFBS position.&amp;lt;br&amp;gt; Conclusions: Our results indicate that direct and selective methylation of certain TFBS that prevents TF binding is restricted to only special cases and cannot be considered as a general regulatory mechanism of transcription.&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Yulia A Medvedeva, Abdullah Khamis, Ivan V Kulakovskiy, Wail Ba-Alawi, Md Shariful I Bhuyan, Hideya Kawaji, Timo Lassmann, Matthias Herbers, Alistair RR Forrest, Vladimir B Bajic and the FANTOM consortium&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;YAM designed the computational experiments, selected and preprocessed the data, produced statistical analysis and wrote the manuscript; AK performed most of the data analysis; WBA and MdSIB contributed RDM models and tools for threshold estimation and mapping; [potential F5 collaborators], IVK performed part of the analysis, contributed to the design of the experiments and writing of the manuscript; VBB contributed to the design of the experiments and writing of the manuscript. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on 50 sample types, ENCODE RRBS data for the same samples &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Genome biology&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;December, 16 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:ju.medvedeva@gmail.com Yulia Medvedeva] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Effect of cytosine methylation on transcription factor binding sites and regulation of transcription.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Effect of cytosine methylation on transcription factor binding sites and regulation of transcription.pdf]] &amp;lt;br&amp;gt;&#039;&#039;&#039;Additional files for general viewing: &#039;&#039;&#039;[[Image:Effect of cytosine methylation on transcription factor binding sites Additional files.zip]] &amp;lt;br&amp;gt;&#039;&#039;&#039;Accepted version: &#039;&#039;&#039; [[Image:Medvedeva et al_ accepted.zip]]&lt;br /&gt;
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== Title: The Evolution of Human Cells in terms of Protein Innovation  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_013 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT MOLECULAR BIOLOGY AND EVOLUTION&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Humans are complex organisms composed of a great many cell types. Since the genomic DNA of each cell is identical, cell type is determined by what is expressed. We examine the evolutionary history of each human cell type at the molecular level via the collective histories of proteins, the principal product of gene expression. Sequence data from the FANTOM5 consortium are used to provide cell-type specific digital expression of protein-coding genes, and the SUPERFAMILY and dcGO resources provide domain and function annotation respectively. Cross-referencing with the domain annotation of all other completely-sequenced genomes provides the evolutionary context for each protein. We combine all of this to generate a description of cellular evolution at the molecular level. &lt;br /&gt;
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We present a protein domain view of the evolution of cell type. To achieve this we first identify the most recent common ancestor (MRCA) or ‘creation epoch’ of every protein in the repertoire of the human genome. We are then able to use the protein creation epochs to describe the history of the emergence of each cell type over evolution in terms of the collective histories of the proteins expressed in that cell type. Each cell type has an evolutionary profile consisting of a timeline along the lineage from the ancient cellular ancestor to modern day human. The profile of each cell type shows at which epochs along the timeline innovations in protein evolution took place; required to allow the observed expression in that type of cell. By clustering cell types on these profiles, we find groups of cell types that share a parallel protein evolutionary history and thus potentially possess a common progenitor cell type or are evolving in cooperation. A functional enrichment analysis of these clusters reveals key proteins responsible for evolutionary shifts and functional innovations; it also suggests a possible order in which different cells could have emerged during evolution, which we discuss in relation to the human immune system. The structural domain-centric perspective which we employ in this work can also be used as the basis for a comparison of the molecular basis of functional and phenotypic differences between cell types within these evolutionary clusters, exemplified by an inspection of our results on different regions of the brain. &lt;br /&gt;
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We present a view of the landscape of nature’s innovation of protein structure and architecture required to explain the creation of the different human cell types. This landscape has some important features such as the possibility that the last universal ancestor of life provided most of the innovation for the innate immune system whilst brain cells have been making use of novel proteins that first appeared in opisthokonta (animals and fungi) and continued to do so right up until homo sapiens. The landscape also lends itself to identifying candidate genes for disease by highlighting those that were important in enabling certain phenotypic shifts at key points in evolution.&amp;lt;br&amp;gt; &lt;br /&gt;
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Authors: &#039;&#039;&#039;Adam J. Sardar, Matt E. Oates, Hai Fang, Alistair R.R. Forrest,Hideya Kawaji, Julian Gough, Owen J.L. Rackham and the FANTOM Consortium&#039;&#039;&#039; &lt;br /&gt;
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Authors contribution statement: FANTOM5 was made possible by a Research Grant for RIKEN Omics Science Center from MEXT to Yoshihide Hayashizaki and a Grant of the Innovative Cell Biology by Innovative Technology (Cell Innovation Program) from the MEXT, Japan to Y.H.. We would like to thank all members of the FANTOM5 consortium for contributing to generation of samples and analysis of the dataset and thank GeNAS for data production. A.J.S. and M.E.O. were funded by BCCS studentships from EPSRC [EP/E501214]; another funding source was the BBSRC [BB/ G022771/1 to J.G., funding O.J.L.R. and H.F.].The authors would like to thank David de Lima Morais for useful discussion at the preliminary stages of this work. &amp;lt;br&amp;gt; Datasets used: &#039;&#039;&#039;Helicos CAGE on all samples &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s):&#039;&#039;&#039;GR&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:gough@compsci.bristol.ac.uk,owen.rackham@gmail.com Julian Gough, Owen Rackham] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Rough draft available on request]] &amp;lt;br&amp;gt; &#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): submitted revisions: [[Full_Manuscript_Sardar_et_al.pdf‎]] &#039;&#039;&#039;[[Image:TraP Journal Submission.zip]]&#039;&#039;&#039; [[Image:GR Submission 3 March Sardar 2013 The Evolution of Human Cells in terms of Protein Innovation.pdf]] &lt;br /&gt;
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== Title:Comparison of CAGE and RNA-seq transcriptome profiling using a clonally amplified and single molecule next generation sequencing  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_027 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT GENOME RESEARCH&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; CAGE (Cap Analysis Gene Expression) and RNA-seq are two major technologies used for transcript quantification. These protocols measure expression by from either the 5’ end of capped molecules (CAGE) or tags randomly distributed along the length of a transcript (RNA-seq). Library protocols for clonally amplified (Illumina, SOLiD, 454, Ion Torrent) 2nd generation sequencing platforms typically employ PCR pre-amplification prior to clonal amplification, while 3rd generation single molecule sequencers can sequence unamplified libraries. While these protocols individually have been demonstrated to be highly reproducible, no systematic comparison has been carried out between the protocols. Here we compare CAGE using both 2nd and 3rd generation sequencers and RNA-seq using a 2nd generation sequencer based on a panel of RNA mixtures from two human cell lines (THP-1 and HeLa, 100%, 50%, 20%, 10%, 5%, 1% and 0% of HeLa RNAs) to examine power to discriminate biological states, to detect differentially expressed genes, linearity of measurements as well as quantification reproducibility. Quantification by CAGE with the 2nd and 3rd generation sequencers (Illumina GA-IIx and HeliScope) were consistent at gene level, however we observed several differences, which can be explained by differences in their protocols and sequencing platforms. These include significant bias in the Illumina library, such as GC biases and over-estimation of transcripts harboring internal Ecop15I sites., A poorer correlation at the level of individual TSS positions, which is likely to be due to higher indel rate in HeliScope, is also found. We found high consistency between HeliScopeCAGE with RNA-seq (spearman correlations 0.88). Differences between CAGE and RNA-seq are explained by incompleteness of existing gene models in most cases, where 5’-ends of gene models do not reflect actual transcription starting site in the profiled cells, or RNA polymerase run through the poy adenylation site resulting in fusion of neighboring genes. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;WP3 &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;Genome Res. &#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: 23rd Dec, 2012 &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Submitted PDF: &#039;&#039;&#039;[[Image:130215-PlatformEval-submittedGR.pdf]]  &lt;br /&gt;
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== Title: Differential roles of epigenetic conversion and Foxp3 expression in regulatory T cell-specific transcriptional regulation  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_029 &amp;lt;br&amp;gt; &lt;br /&gt;
&#039;&#039;&#039;Status: ACCEPTED AT PNAS&#039;&#039;&#039;&amp;lt;br&amp;gt;&lt;br /&gt;
&#039;&#039;&#039;Abstract: &#039;&#039;&#039;Naturally occurring regulatory T (Treg) cells are engaged in the maintenance of immune tolerance and homeostasis. The development of Treg cells requires both the expression of the transcription factor Foxp3 and the establishment of Treg cell-type DNA hypomethylation pattern. By transcriptional start site (TSS) cluster analysis, we here assessed possible correlation of genome-wide DNA methylation pattern or Foxp3-binding pattern with Treg-specific gene expression. We found that Treg cell-specific DNA hypomethylated regions were closely correlated with Treg-upregualted TSS clusters, whereas Foxp3-binding regions had no significant correlation with either up- or down-regulated clusters, in non-activated Treg cells. On the other hand, in activated Treg cells, Foxp3-binding regions showed a strong correlation with down-regulated clusters. In silico search for transcription factor-binding motifs revealed that the motifs enriched in Foxp3-binding or Treg-specific DNA hypomethylated regions were mostly different. These results collectively indicate that Treg cell-specific DNA hypomethylation is conducive to up-regulation in the steady state Treg cells whereas Foxp3 expression to down-regulation of its target genes in activated Treg cells. Thus, the combination of the two events is required for the establishment of Treg cell-specific gene expression and function. &lt;br /&gt;
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(185 words)&amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Authors: &#039;&#039;&#039;Hiromasa Morikawa1,2, Naganari Ohkura1, Alexis Vandenbon3, RIKEN_OSC_members 4, Daron Standley3, Hiroshi Date2, Shimon Sakaguchi1 &lt;br /&gt;
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1. Department of Experimental Immunology, World Premier International Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan&amp;lt;br&amp;gt;2. Department of Thoracic Surgery, Kyoto University, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan&amp;lt;br&amp;gt;3. Department of Systems Immunology, World Premier International Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan&amp;lt;br&amp;gt;4. RIKEN Omics Center, Yokohama, Japan&amp;lt;br&amp;gt;&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &amp;amp;nbsp;Genome Research&#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &amp;amp;nbsp;2012/12/18&#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:hmorikawa@ifrec.osaka-u.ac.jp Hiromasa Morikawa] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: [https://fantom5-collaboration.gsc.riken.jp/wiki/index.php/File:Submit130114v3.docx Submit130114v3.docx]&#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF):&amp;amp;nbsp;[https://fantom5-collaboration.gsc.riken.jp/wiki/index.php/File:Submit130114v3.pdf Submit130114v3.pdf]&#039;&#039; &lt;br /&gt;
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== Title: An atlas of active enhancers across human cell types and tissues  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_35 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT NATURE&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; In higher organisms, cellular development and diversity is highly controlled by enhancers, which regulate the correct temporal and cell type-specific activation of gene expression. Despite their obvious importance for development and disease, the exact locations, target genes and mechanisms of enhancers are still poorly defined. Thus, there is an urgent need not only to identify enhancer locations, but also to elucidate their specific usage across the wide diversity of cells within the human body, their impact on regulation in healthy and diseased individuals, and how enhancers interact with target genes. Here, we use the FANTOM5 panel of tissue and primary cell samples covering the majority of human tissues and cell types to define an atlas of active, in vivo bidirectionally transcribed enhancers across the human body. It enables comparison of regulatory programs between different cells and tissues at unprecedented depth, and makes it possible to define distinct subsets of enhancers, including fetal-specific, cell-specific and ubiquitous enhancers – a novel enhancer subtype with distinct properties. We show that known target genes of enhancers can be recaptured using expression correlations and predict many novel enhancer-TSS associations. We present models confirming the utility of multiple redundant enhancers, which explain TSS expression strength rather than expression patterns. We demonstrate that disease-associated functional single nucleotide polymorphisms are over-represented in enhancers and that such enhancers often have disease-relevant expression patterns. The human enhancer atlas can be accessed through an online database and is a unique resource for studies on tissue/cell-specific enhancers and their gene interactions. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Robin Andersson1#, Claudia Gebhard2#, Irene Miguel-Escalada3, Ilka Hoof1, Xiaobei Zhao1, Christian Schmidl2, Eivind Valen1,4, Kang Li1, Lucia Schwarzfischer2, Dagmar Glatz2, Johanna Raithel2, Yun Chen1, Berit Lilje1, Nicolas Rapin1,5, Frederik Otzen Bagger1,5, Mette Jørgensen1, Mette Boyd1, Jette Bornholdt1, Kenneth Baillie6, Chris Mungall7, Timo Lassmann8, Hideya Kawaji8, Andreas Lennartsson9, Carsten Daub8,9, David Hume6, Peter Heutnik10, Alistair Forrest8, Piero Carninci8, Yoshihide Hayashizaki8, Ferenc Müller3, Michael Rehli2*, Albin Sandelin1* &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;RA, IH, EV, KL, YC, BL, XZ, MJ, HK, TL, KB, CM, NR, FOB, MR, AS made the computational analysis. TL, HK, CD, AF, PC, YH prepared, mapped and analyzed CAGE libraries. RA, CG, IH, EV, FM, PC, AF, AK, MB, JBL, AL, CD, DH, PH MR, AS interpreted results. CG, CS, ME, MR made the blood cell ChIP experiments, methylation assays and in vitro blood cell validations. IME, FM made zebrafish in vivo validations and interpretations. RA, CG, IH, FM, MR, AS wrote the paper. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks and raw CAGE mapped data from human, internal ChIP and other validation data &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; To be decided &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[robin@binf.ku.dk, michael.rehli@klinik.uni-regensburg.de, albin@binf.ku.dk , Michael Rehli Albin Sandelin] &amp;lt;br&amp;gt; &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] [[Image:Enhancerome full.pdf]]&#039;&#039;&#039; &lt;br /&gt;
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== Title: Analysis of DNA methylation and transcription during granulopoiesis reveals timed methylation changes in low CpG areas and regulation of transcription factor expression and motif activity  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_001 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;In development epigenetic mechanisms such as DNA methylation have been suggested to provide cellular memory to maintain pluripotency but also stabilize cell fate decisions and direct lineage restriction. In this study we set out to characterize changes in DNA methylation levels and gene expression during granulopoiesis using four distinct cell populations ranging from the oligopotent common myeloid progenitor stage to terminally differentiated neutrophils. We found a general decrease of DNA methylation during granulopoiesis. Methylation levels appear to change at specific differentiation stages and correlate with changes in transcription and motif activity of key hematopoietic transcription factors. Differentially methylated sites (DMSs) are preferentially located in areas distal to CpG islands and shores and are overrepresented in potentially regulatory enhancer elements. Overall this study depicts in detail the epigenetic and transcriptional changes that occur during granulopoiesis and supports the role of DNA methylation as a regulatory mechanism in cell differentiation. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Michelle Rönnerblad, Tor Olofsson, Sören Lehmann, RIKEN_OSC_members, Karl Ekwall*, Erik Arnér* &amp;amp;amp; Andreas Lennartsson* &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did most of the practical experiments, the bioinfo analysis (except CAGE related) and most manuscript writing, TO isolated the cells from bone marrows, SL gave valuable input to the planning, analysis and critically reviewed the manuscript, KE planned and supervised the study and contributed to the manuscript writing , EA supervised the bioinformatic analysis and performed the ones related to CAGE and contributed to the manuscript writing, AL initiated, planned and supervised the study and contributed to the manuscript writing and did some experiments. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on granulo precursor populations &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Blood &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;April 7th 2012 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:andreas.lennartsson@ki.se,Karl.Ekwall@ki.se,arner@gsc.riken.jp andreas lennartsson, Karl Ekwall, Erik Arner] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Rönnerblad.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Rönnerblad Aprl07.pdf]] &lt;br /&gt;
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== Title: Ceruloplasmin is a Novel Adipokine Which is Overexpressed in Adipose Tissue of Obese Subjects and in Obesity-Associated Cancer Cells  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_32 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT PLOS ONE&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; Obesity confers an increased risk of developing specific cancer forms. Although the mechanisms are unclear, increased fat cell secretion of specific proteins (adipokines) may promote/facilitate development of malignant tumors in obesity by cross-talk between adipose tissues and the tissues prone to develop cancer among obese. This was investigated using expression data from human adipose tissue of obese and non-obese as well as from a large panel of human cancer cell lines and corresponding primary cells and tissues. We identified three previously described adipokines, SERPINE1, SERPINE2 and C3 sharing a common cognate receptor LRP1 which was expressed in all cancer cell lines associated with obesity. Expression and secretion of SERPINE1 and C3 were increased in obese adipose tissue and their plasma levels were elevated in obese subjects. We also identified genes enriched in obesity-associated cancer cells compared to cell lines and corresponding healthy tissues or primary cells. We found expression of ceruloplasmin to be the most enriched in obesity-associated cancer cells. This gene was also significantly up-regulated in adipose tissue of obese subjects. Ceruloplasmin is the body’s main copper carrier and is involved in angiogenesis. We demonstrated that ceruloplasmin was a novel adipokine and that obese adipose tissue contributed markedly (22%) to the total protein level. In summary, we have identified several adipokines, which can serve as endocrine signals facilitating growth of obesity-associated cancer tumors. These adipocyte signals are increased in obesity and may be important for development of cancer associated with excess body fat. &lt;br /&gt;
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&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Erik Arner, Alistair Forrest, Anna Ehrlund, Niklas Mejhert, [Additional RIKEN people?], Jurga Laurencikiene, Mikael Rydén, Peter Arner &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s):&#039;&#039;&#039; Cancer Research &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:arner@gsc.riken.jp Erik Arner] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Fat cells and cancer draft 120816 EA.docx]] [[Image:Figs 2012-08-15.ppt]]&amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039; &lt;br /&gt;
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== Title: Interactive visualization and analysis of large-scale NGS data-sets using ZENBU  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_33 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT NATURE BIOTECHNOLOGY&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039;The world of genome sciences has dramatically changed over the last 5 years. With the advent of next generation sequencers and RNA-expression sequencing, genome science is no longer the domain of a few elite centralized &amp;quot;genome centers&amp;quot; like in the early days of the field. The advance of next-generation sequencers has spurred an ever-growing body of tag-based data allowing the survey of chromatin states and transcriptome dynamics. Visualization of expression levels of genomic regions was achieved by displaying expression levels in various experimental conditions in dedicated tracks allowing investigators a direct comparison of their dynamics. Novel file formats and browser design have allowed for dealing efficiently with the depth of data produced by next-generation sequencer based technologies. Researchers need to interact within global collaborations and need easy ways to process, share and visualize their data in a secured manner prior to publication. To this end we have developed the ZENBU system. ZENBU is a web based system which is a social networking platform for secured data upload and data sharing with collaborators, a data processing system, and a visualization system. ZENBU provides the infrastructure for working with 100s of terrabytes of sequence data in the form of BAM sequence alignment files and genome annotation formats like BED and GFF, to efficiently cross-analyze these databsets using a Map-Reduce/autonomous-agent based parallel processing system, and provide fast efficient web services for user interfaces. The user interfaces for ZENBU is based on Web2.0 technologies in the form of a new expression-enhanced genome browser, and data manipulation interfaces for data upload, data processing, and data download. ZENBU currently contains the entire FANTOM 3/4/5 datasets, the entire ENCODE datasets, and much of the UCSC genome annotation data. ZENBU is planned to be a corner stone in the expanding global network of scientific sharing web systems.&amp;lt;br&amp;gt; &lt;br /&gt;
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&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Jessica Severin*, Marina Lizio, Jayson Harshbarger, Hideya Kawaji, Carsten Daub, The FANTOM5 consortium, Yoshihide Hayashizaki, Nicolas Bertin*, Alistair Forrest* &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement:&#039;&#039;&#039; &#039;&#039;JMS, ML, JH, HK, CD, YH, NB, AL&#039;&#039; &lt;br /&gt;
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*JMS, wrote the software/webservices. &lt;br /&gt;
*JMS, NB, planned the study. &lt;br /&gt;
*NB supervised the study. &lt;br /&gt;
*JMS, NB, contributed to the manuscript writing. &lt;br /&gt;
*JMS, NB, gave valuable input to the analysis in the manuscript. &lt;br /&gt;
*JMS, NB, critically reviewed the manuscript. &lt;br /&gt;
*&#039;&#039;[addition of any other, clearer or more precise statement is very welcome]&#039;&#039;&lt;br /&gt;
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&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s):&#039;&#039;&#039; Nature Biotech/Genome Research &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:severin@gsc.riken.jp,nbertin@gsc.riken.jp,forrest@gsc.riken.jp Jessica Severin, Nicolas Bertin, Alistair Forrest] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of the most up to date manuscript draft: &#039;&#039;&#039;[[Image:ZENBU manuscript.014 (1).docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Cell-type specificity and co-expression of regulatory polymorphisms associated with human disease  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_002 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO GENOME RESEARCH&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Our ability to use genetic associations with disease to develop better treatments has been limited by the difficulty of identifying a biological process, or cell type, on which to focus investigation. Most disease-associated polymorphisms do not lie within protein-coding genes, raising the possibility that variation in regulatory sequence plays a critical role in disease phenotypes. We have used genome-scale 5’RACE (CAGE) to identify the location and usage of transcription start sites in 864 human tissues, primary cells and cell lines, and show here that there is a strong enrichment for disease-associated variants within the sequence immediately adjacent to transcription start sites. Using the expression profiles of known variants associated with disease susceptibility, we identify experimentally-available cell types significantly associated with specific diseases and traits. The expression of genes known to be associated with particular diseases was positively correlated. Such co-expression was used to identify unreported candidate disease-associated regulatory regions within published genome-wide association studies (GWAS). The approach was validated by identifying candidate loci in a 2007 GWAS study that were subsequently validated in larger independent datasets These functional genomics approaches directly inform choices of model system and identify disease- and cell type-specific co-regulated networks for a wide range of common diseases. &lt;br /&gt;
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&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Baillie JK*, Haley CS, Schaefer U, Faulkner GJ, Freeman T, Brown JB, [others...], [Numerous RIKEN authors, order etc. TBC, at least including: Kawaji H, Forrest A, Carninci P]*, Hume DA* &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on Primary Cells &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Nature Genetics &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; ...&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:j.k.baillie@ed.ac.uk,david.hume@roslin.ed.ac.uk Kenneth Baillie, David Hume] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Ab Initio Prediction of Tissue-Specific Regulatory Modules in the FANTOM5 Project  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_005 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO GENOME RESEARCH&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;One of the major goals of the FANTOM5 project, the broadest TSS-based promoter-level expression atlas of transcriptional regulatory networks, is the identification of coding and non-coding, annotated and novel transcriptional units being transcribed in a cell-specific mode across the different biological states/samples. In this work we analyzed the FANTOM5 dataset using ScanAll, a newly developed software here described, to ab initio predict the presence of conserved elements in the genomic regions surrounding FANTOM5 promoters. Firstly we aimed at identifying motifs that were conserved in a subset of the selected genomic regions and that possibly corresponded to Transcription Factor Binding Sites (TFBS); we then expanded our analysis to pinpoint the existence of more complex, structured regulatory modules, that is groups of conserved motifs co-occurring in the aforementioned (co-expressed) regions within a fixed distance. We confirmed the sample-specificity of our output by showing that the majority of the obtained combinations of modules were able to divide the specimens into sample-specific groups, thus possibly explaining the peculiarities of regulatory events occurring in each tissue. Among these sites it was possible to confirm the presence of TFBS for known regulators already associated to those samples together with an additional and significant portion of motifs remaining unannotated, thus representing putative novel binding elements. In addition we were able to associate the presence of a significant portion of the identified motifs to distinct families of repeated elements, thus confirming a structural/functional feature of mammalian promoters that is currently emerging as one of the most peculiar regulatory aspects associated to mammalian phylogeny. Finally, we were able to identify previously uncharacterized aspects of the regulatory networks occurring in early-development samples thus confirming the significant advantage deriving from our modular approach. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Emiliano Dalla, Yari Ciani, Marco Zantoni, Alberto Policriti, Hideya Kawaji, Michiel J.L. de Hoon, Timo Lassmann, Alistair R.R. Forrest, Michael Rehli, Ivan Kulakovsky, Claudio Schneider, Silvano Piazza &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;ED conceived the project, developed part of the software, oversaw implementation, performed some of the analysis and most manuscript writing; YC implemented part of the software, performed some of the analysis and prepared some figures; MZ developed and implemented part of the software; AP developed part of the software and contributed to the manuscript writing; TL was responsible for tag mapping; HK managed the data handling; MR, IK and MJLdH were involved in motif assessment; ARRF was responsible for FANTOM5 management and concept; CS supervised the study; SP developed and implemented part of the software, carried out statistical tests and results interpretation and wrote parts of the manuscript. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on all of F5freeze1 &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;June 1st 2012; Update: December 21st 2012: Post Internal Review Update: January 28th 2012 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:emiliano.dalla@lncib.it Emiliano Dalla] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:FANTOM5 PromoteromeSatelliteLNCIB.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:FANTOM5 PromoteromeSatelliteLNCIB wFigures.pdf]] &lt;br /&gt;
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== Title: A high resolution spatial-temporal promoterome of the human brain (was Brain CAGE)  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_007 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO GENOME RESEARCH&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;The human brain is an extremely complex organ that governs our abilities for cognition, reasoning and emotions and is the control center for the body. Its morphology and functionality during development have been well studied, but the molecular mechanisms contributing to its function and maintenance later in life remain poorly understood. Complexity at the transcriptional level is likely to play a major role in defining its morphological and functional characteristics. To investigate this we used single molecule CAGE and created a high resolution atlas of transcription start sites for 15 anatomical regions of the human central nervous system, using post-mortem samples derived from infant and aged adult donors. On the transcriptional level brain is clearly distinguishable from other tissues even if we consider only non-coding genes or expression from genomic regions often described as genomic dark matter. Using these differences we identify a specific set of transcription start sites that characterizes the brain. We show extensive differences in transcription between infant and adult that in some cases can be linked to loci associated with major neurodegenerative diseases. The differential expression across distinct regions correlates well with developmentally and/or functionally related anatomical districts and is refelected by distinct networks of interacting transcription factors, a range of lncRNAs and novel transcripts co-expressed in a regionally biased manner. Overall we provide the scientific community with a powerful expression resource based on post-mortem tissue, particularly highlighting the contribution of non-coding RNAs to the transcriptional complexity of human central nervous system. &lt;br /&gt;
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&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Margherita Francescatto, Morana Vitezic, Patrizia Rizzu, Javier Simon-Sanchez, Robin Andersson, FANTOM5_RIKEN_OSC_members, Carsten O Daub, Albin Sandelin, MIchiel JL de Hoon, Piero Carninci, Alistair RR Forrest, Peter Heutink &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MF and MV did the analyses; MF, MV and PH wrote the manuscript, PR selected all samples, evaluated medical and pathological records and isolated RNA, JSS curated the list of disease loci, RA and AS provided the list of enhancers, ARRF, PC and PH designed the study ... &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on VUMC provided brain samples (adult and newborn); full list of samples presented in Supplementary Table 1&amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Genome Research &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Peter.Heutink@dzne.de,m.francescatto@vumc.nl,mvitezic@gsc.riken.jp Peter Heutink, Margherita Francescatto, Morana Vitezic] &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Final version: &#039;&#039;&#039;[[Image:Francescatto and Vitezic manuscript.pdf]] [[Image:Francescatto and Vitezic figures.pdf]] [[Image:Francescatto and Vitezic Supplementary Note.pdf]]&amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Chromatin states reveal functional associations for globally defined transcription start sites in four human cell lines  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_017&amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO BMC GENOMICS&#039;&#039;&#039; &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: Background: &#039;&#039;&#039;Deciphering the most common modes by which chromatin regulates transcription, and how this is related to cellular status and processes is an important task for improving our understanding of human cellular biology. The FANTOM5 and ENCODE projects represent two independent large scale efforts to map regulatory and transcriptional features to the human genome. Here we investigate chromatin features around a comprehensive set of transcription start sites in four cell lines by integrating data from these two projects. &#039;&#039;&#039;Results:&#039;&#039;&#039; Transcription start sites can be distinguished by chromatin states defined by specific combinations of both chromatin mark enrichment and the profile shapes of these chromatin marks. The observed patterns can be associated with cellular functions and processes, and they also show association with expression level, location relative to nearby genes, and CpG content. In particular we find a substantial number of repressed inter- and intra-genic transcription start sites enriched for active chromatin marks and Pol II, and these sites are strongly associated with immediate-early response processes and cell signaling. Associations between start sites with similar chromatin pattern are validated by significant correlations in their global expression profiles. &#039;&#039;&#039;Conclusions:&#039;&#039;&#039; The results confirm the link between chromatin state and cellular function, but they also show that the relationship between chromatin state and transcription is more subtle than previously appreciated. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Morten Rye, Geir Kjetil Sandve, Finn Drablos&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR, GKS and FD did data analysis and wrote the paper&amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE data, ENCODE chromatin ChIP-Seq and DNase HS data&amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Genome Biology &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;01.03.2013&amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:finn.drablos@ntnu.no,morten.rye@ntnu.no Finn Drablos,Morten Rye]&amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Internal submission draft FD GKS MBR 010313.docx]] &amp;lt;br&amp;gt; &#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Main figures 01032015.pdf]] &#039;&#039;&#039;Supplementary figures: &#039;&#039;&#039;[[Image:All supplem figs 01032013.pdf]] &lt;br /&gt;
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== Title: Evolution of expression patterns in human gene families illustrated by the FANTOM5-CAGE encyclopedia of transcription start sites.  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_019 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO BMC EVOLUTIONARY BIOLOGY&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &lt;br /&gt;
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Background Human gene families emerged through consecutive rounds of gene duplication. Here we apply the cutting-edge FANTOM5 single-nucleotide resolution atlas of transcription start sites from 1348 human and mouse libraries, to elucidate expression pattern evolution in animal gene families, with stress on comparison between human and mouse, and normal versus cancer cells. &lt;br /&gt;
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  Results  Broad over-view of FANTOM5 was obtained with intra-species and inter-species hierarchical clustering of human and mouse samples. In the follow-up, we dated gene duplications by phylogenetic timing, and investigated the rate of expression pattern divergence between duplicates, as well as the tissue-specificity of their expression. Finally, we defined the concept of phylo-expression signatures as strong associations between duplications of certain ages and expression samples in the FANTOM5 atlas. We show how phylo-expression signatures can be used to generate novel hypotheses on the nature of animal evolution, and discuss central nervous system and reproductive tract as two focused examples.   &lt;br /&gt;
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Conclusions A striking trend for young genes to be narrowly expressed was revealed. Several lines of evidence suggested that emergence of placental mammals was a unique period in the evolution of animal gene families and duplicates dating to that period have broader and more conserved expression patterns, with genes involved in chromatin assembly and epigenetic control driving the trend. A major strength of the FANTOM5 atlas is that it profiles normal tissues, primary cells, and cancer cell lines, and as expected, clustering of expression profiles showed a major divide between leukemias and solid tumors. Where the evolutionary link became apparent was that in cancer cell lines, unlike in tissues and primary cells, recent paralogs lacked the peak of highly correlated pairs. This novel finding suggests that global devolution and loss-of-evolutionary constraints on expression patterns accompany malignant transformation, and provides additional evidence in the debate on use of cancer cell lines as research models. &lt;br /&gt;
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&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;&amp;lt;br&amp;gt; OS and LH designed the study, performed all analyses, and wrote the manuscript. &amp;lt;br&amp;gt; A.R.R.F. and C.O.D were involved in the FANTOM5 concepts and management. &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE, TreeFam8&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Biology&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: November 30th&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Lukasz.Huminiecki@ki.se Lukasz Huminiecki] ,[mailto:oxana.sachenkova@scilifelab.se Oxana Sachenkova] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors&amp;amp;nbsp;: &#039;&#039;&#039;[[Image:The structure of animal expression pattern evolution.doc]] (only text)&amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:The structure of animal expression pattern evolution.pdf]] (this file includes all the figures) &lt;br /&gt;
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== Title:Automated clustering and quality control pipeline for CAGE technologies  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_030 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO BMC GENOMICS&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; To understand the manner and mechanisms of transcription initiation by RNA Polymerase II, different strategies for genome-wide detection of transcription start sites (TSSs) have been developed. We propose the clustering and quality control pipeline suitable for the Cap Analysis of Gene Expression (CAGE) sequence tags. The new framework uses parametric clustering at multiple scales and adopts the irreproducible discovery rate (IDR) to measure reproducibility between replicates of each cluster. Our pipeline reveals that genes have complicated structures of transcription initiation events and discover novel alternative promoters which were not detected by previous approaches. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039; Hiroko Ohmiya1, Morana Vitezic1, Martin Frith, Yoshihide Hayashizaki1, Timo Lassmann1 and many more &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:lassmann@gsc.riken.jp Timo Lassmann] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Manuscript Ohmiya Mar04.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Manuscript Ohmiya Mar04.pdf]] [[Image:Additional file2.txt]] &lt;br /&gt;
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== Title: Mesenchymal stem/stromal cells from high-grade serous ovarian cancer retain specific identity related to mesothelium  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_036 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO STEM CELLS&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;The role of cancer microenvironment is being recognized as one of the critical hallmarks in both cancer progression and metastasis. Mesenchymal Stem/Stromal Cells (MSCs) are the precursors of various cell types that compose both normal and cancer tissue microenvironments. We have isolated MSCs from various High-Grade Serous Ovarian Carcinomas (HG-SOCs), demonstrated their normal genotype, and analyzed their transcriptome with respect to similarly derived normal tissues MSCs (N-MSCs), all embedded in the large comprehensive FANTOM5 sample dataset. An integrative analysis was conducted against the extensive panel of primary cells and tissues of the FANTOM5 project that allowed us to identify a cell-type specific transcriptional activity associated with the HG-SOC-MSCs. In fact the analysis shows that HG-SOC-MSCs retain a specific identity when compared to N-MSCs and are related to the primary mesothelial or mesothelial-derived cells representing the ovarian cellular precursors. Our results support the hypothesis that HG-SOC-MSCs are bona-fide representatives of the ovarian district thus tracing their origin either to the local mesothelium or highlighting the epigenetic conditioning of externally recruited MSCs by the HG-SOC cancer cell compartment. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Roberto Verardo, Silvano Piazza, Enio Klaric, Yari Ciani, Stefania Marzinotto, Laura Mariuzzi, Daniela Cesselli, Antonio P. Beltrami, Masayoshi Itoh, Hideya Kawaji, Timo Lassmann, Piero Carninci, Yoshihide Hayashizaki, Alistair R.R. Forrest, Carlo A. Beltrami, Claudio Schneider and the FANTOM consortium &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;R.V., S.P. and C.S. designed research and analyzed all the data; R.V. followed all sample RNA/DNA quality controls; S.P. designed software, carried out statistical tests and bioinformatics analysis; Y.C. implemented part of the software and prepared some figures; E.K. performed molecular biology assays; R.V., S.M., L.M., D.C., and A.P.B. performed cell isolation and characterization, R.V., D.C., A.P.B., C.A.B. and C.S. analyzed cell-biology data; M.I. was responsible for CAGE data production; T.L. was responsible for tag mapping; H.K. managed the data handling; P.C., Y.H. and A.R.R.F. were responsible for FANTOM5 management and concept; CS supervised the whole study; R.V., S.P. and C.S. wrote the manuscript. &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on all of F5freeze1 &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;October 15th 2012 &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:schneide@lncib.it Claudio Schneider] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Claudio.pdf]] &lt;br /&gt;
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== Title: A transient disruption of a fibroblast-specific transcriptional regulatory network potently promotes trans-differentiation  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_40&amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO GENOME BIOLOGY &#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; Background: Transcriptional Regulatory Networks (TRN) coordinates multiple transcription factors (TF) in concert to maintain homeostasis and cellular function. The re-establishment of TRNs have been previously implicated in direct trans-differentiation studies where the newly introduced TFs switch-on a set of key regulatory factors to induce de novo expression and function. However, the extent to which TRNs in starting cell types, such as dermal fibroblasts, protect the cells from undergoing cellular reprogramming remains largely unexplored. Results: In order to identify specific TFs in fibroblasts, we first modeled the TRN of fibroblast cells using a Matrix-RNAi approach where 18 fibroblast-specific TFs were systematically knock-downed and profiled. The resulting expression matrix revealed 7 highly interconnected TFs as targetable factors. Interestingly, suppressing 4 out of 7 TFs generated lipid droplets and induced PPARG and CEBPA expression in the presence of adipocyte-inducing medium, while the control knockdown maintained fibroblastic characteristics in the same induction regime. The global gene expression analysis further revealed that the knockdown induced adipocytes (KDiADP) highly expressed genes associated with lipid metabolism and significantly suppressed fibroblast-specific genes. Conclusion: Overall, this study reveals the critical role of the TRN in protecting cells against aberrant reprogramming, and demonstrates, for the first time, the vulnerability of TRN, which may be a novel target to induce transgene-free trans-differentiations.  &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: Yasuhiro Tomaru, Ryota Hasegawa, Jay W. Shin , Takahiro Suzuki, Taiji Sato, Atsutaka Kubosaki, Masanori Suzuki, Yoshihide Hayashizaki and Harukazu Suzuki&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;YT designed and carried out experiments, analyzed and wrote the paper. RH carried out experiments, supported statistical analysis and wrote the paper. JS generated expression data, analyzed and wrote the paper. TS, TS and AK carried out validation of KDiADP cells. MS carried out editing of the manuscript. YH and HS coordinated all efforts and supervised the project&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Biology&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: May 20th, 2013&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:harukazu@gsc.riken.jp]Harukazu Suzuki, [mailto:jay.shin@gsc.riken.jp]Jay Shin&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:manuscript-YT-May17.docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Tomaru_F5_wiki.pdf]] &lt;br /&gt;
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== Title: Explaining the correlated properties of mammalian promoters  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_003 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Advanced draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;Proximal promoters are fundamental genomic elements for gene expression. They vary in terms of: GC percentage, CpG abundance, presence of TATA signal, evolutionary conservation, chromosomal spread of transcription start sites, and breadth of expression across cell types. These properties are correlated, and it has been suggested that there are two classes of promoter: one class with high CpG, widely spread transcription start sites, and broad expression, and another with TATA signals, narrow spread and restricted expression. It has been unclear, however, why these properties are correlated in this way. &lt;br /&gt;
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We re-examined these features using the deep FANTOM5 CAGE data from hundreds of cell types. Firstly, we point out subtle but important biases in previous definitions of promoters and of expression breadth. Secondly, we show that most promoters are rather non-specifically expressed across many cell types. Thirdly, promoters&#039; expression breadth is independent of maximum expression level, and therefore correlates with average expression level. Fourthly, the data show a more complex picture than two classes, with a network of direct and indirect correlations among promoter properties. By distinguishing the direct from the indirect correlations, we reveal simple explanations for them. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;M.C. Frith, ...? &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;All human and mouse Phase1 CTSSs &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Research(?) &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;Feb 2013 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:martin@cbrc.jp Martin Frith] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Mcf-prom-sat.pdf]] &amp;lt;br&amp;gt;&#039;&#039;&#039;Supplement: &#039;&#039;&#039;[[Image:Mcf-prom-sat-sup.pdf]] &lt;br /&gt;
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== Title: Homotypic clusters of transcription factor binding sites in the vicinity of transcription start sites  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_006 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Finished draft&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;Background&#039;&#039; &amp;lt;br&amp;gt;Transcription factors (TFs) specifically recognizing DNA binding sites (TFBS) play a key role in regulation of gene expression. Groups of closely localized TFBSs for a particular TF, so-called homotypic TFBS clusters (HCBSs), were originally detected in yeast and extensively studied in fruit fly early development. Recently HCs were found to be highly important for several human regulatory systems. &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;Motivation&#039;&#039; &amp;lt;br&amp;gt;It is a general practice to estimate an enrichment of binding sites in regulatory sequences. Still there is no systematized data whether the presence of HCBSs is common for promoter regions of human genes. The general properties of HCBSs also remain unclear as well as possible relation between HCBSs and regulation of tissue-specific expression. &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;Results&#039;&#039; &amp;lt;br&amp;gt;Using data on sample-specific transcription start sites (TSSs) detected in FANTOM5 and high quality binding models for more than 400 TFs from the HOCOMOCO TFBS model collection we have predicted TFBSs and corresponding HCBSs in promoter regions surrounding TSSs. TFBS models for most TFs were shown to form statistically significant HCBSs often formed by separate distant binding sites. For HCBSs of most of TFs we were able to identify samples having significant association between promoters of sample-specific or housekeeping TSSs. Thus for most of TFs we predict putative preferences for sample-specific or housekeeping HCBSs activity and provide a genome-wide map of HCBSs nearby FANTOM5-defined TSSs. &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;Supplementary information&#039;&#039; &amp;lt;br&amp;gt;https://fantom5-collaboration.gsc.riken.jp/webdav/home/vigg/homotypicus/ &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Authors: &#039;&#039;&#039;I.V. Kulakovskiy, Y.A. Medvedeva, M.S. Polishchuk, A.V. Favorov, S. Schmeier, T. Lassman, I.E. Vorontsov, RIKEN_OSC_members, V.J. Makeev &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039; IVK implemented the software and drafted the manuscript. YAM carried out statistical tests and results interpretation. MSP developed the homotypic cluster detection algorithm. AVF selected proper statistical tests. SS provided the housekeeping set of TSS-clusters. TL provided the set of sample-specific TSS-clusters. IEV estimated proper thresholds for PWMs used in the study. VJM coordinated the study. All the authors participated in writing and finalizing the manuscript. &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE - FANTOM5 FREEZE1, &amp;quot;robust&amp;quot; subset &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Nucleic Acids Research, Bioinformatics &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;18 June 2012 / Updated: 12 September 2012 / Minor fixes: 1 December 2012&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:vsevolod.makeev@gmail.com,ivan.kulakovskiy@gmail.com Vsevolod Makeev, Ivan Kulakovskiy] &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:HOMOTYPICUS-FANTOMsatellitepaper.r1.doc]] &amp;lt;br&amp;gt; &#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:HOMOTYPICUS-FANTOMsatellitepaper.r1.pdf]] &lt;br /&gt;
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== Title: Transcriptional profiling by deep CAGE of the human fibrillin/LTBP gene family, key regulators of mesenchymal cell functions.  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID&#039;&#039;&#039;: Phase1_014 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Good Draft &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; The fibrillins and latent transforming growth factor binding proteins (LTBPs) form a superfamily of extracellular matrix (ECM) proteins characterized by the presence of a unique domain, the 8-cysteine transforming growth factor beta (TGFβ) binding domain (TB domain). These proteins are involved in both maintaining the extracellular matrix and controlling the bioavailability of TGFβ family members. Genes encoding these proteins show differential expression in mesenchymal cell types which synthesise the extracellular matrix and form connective tissues. We have investigated the promoter regions of the seven gene family members using the FANTOM5 CAGE data base for human. Although the protein and nucleotide sequences show considerable homology, the promoter regions were quite diverse. The three fibrillin genes had a single predominant promoter cluster, while LTBP1 and LTBP4 showed promoter switching. Most of the family members were expressed in a range of mesenchymal and other cell types, often associated with use of alternative promoters or transcription start sites within a promoter. FBN3 was the lowest expressed gene, and was expressed only in embryonic and fetal tissues, primarily neurological. There was evidence of enhancer activity likely to be involved in expression of the genes. Each gene showed a unique pattern of transcription factor motifs or activity. This study highlights the role of alternative transcription start sites in regulating the tissue specificity of closely related genes and suggests that this important class of extracellular matrix genes is subject to subtle regulatory variations that explain the differential roles of members of this gene family.&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors:&#039;&#039;&#039; Margaret R Davis, RIKEN OSC members, Kim M Summers&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement:&#039;&#039;&#039; MRD performed the analysis and contributed to writing the paper, RIKEN OSC did ..., KMS performed the analysis and contributed to writing the paper&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used:&#039;&#039;&#039; Helicos CAGE on ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s):&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &amp;lt;br&amp;gt;Contact by email: &#039;&#039;&#039;[mailto:kim.summers@roslin.ed.ac.uk kim.summers@roslin.ed.ac.uk]&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors:&#039;&#039;&#039; [[File:Fantom5_FBN_paper_22-08-13.doc]], [[File:Supplementary_Table_1.pdf]], [[File:Supplementary_Table_2.xlsx]], [[File:Supplementary_Table_3.xlsx]], [[File:Supplementary_Table_4.xls]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF):&#039;&#039;&#039; [[Image:Fibrillin-LTBP satellite.pdf]]&amp;lt;br&amp;gt;&#039;&#039;&#039;Revised version of paper:&#039;&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
[[Image:Summers Phase1 014 revision 18Apr2013.pdf]] &lt;br /&gt;
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&lt;br /&gt;
== Title: Analysis of antisense transcription in loci associated to neurodegenerative diseases  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_022 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;The FANTOM5 sequencing datasets represent the largest collection of transcriptomes from human cell lines, primary cells and whole tissues of various origin. Transcription starting sites are mapped at high resolution by the use of a modified protocol of Cap-Analysis of Gene Expression (CAGE) for high-throughput single molecule next-generation sequencing with Helicos (hCAGE). We employed the FANTOM5 collection of data to address the role of antisense transcription in neurodegeneration. We focused our analysis exclusively on tissues and primary cells, to avoid artifacts due to cellular transformation in culture cell lines. Among the &amp;amp;gt;1261 human hCAGE libraries, we selected those of brain origin. Libraries from total blood and selected blood cell populations were also included in the analysis. A total of 66 tissue- and 244 cell-specific libraries were interrogated for the presence of antisense transcription to well-established loci associated to Alzheimer’s disease, Amyotrophic Lateral Sclerosis, Frontotemporal Dementia, Huntington’s and Parkinson’s disease. Almost all analyzed genes display some degree of antisense transcription mainly in their 5’ or 3’ UTRs. 5’ head-to-head divergent antisense transcription appears enriched compared to global distribution of sense/antisense pairs. Identified antisense transcripts may have coding and non-coding capabilities, with lncRNAs being more represented. Expressed transcripts are generally poorly annotated and may contain repetitive elements of the Alu, SINE and LINE families. Antisense transcription was validated for a subset of genes, including amyloid precursor protein, microtubule-associated protein tau, DJ-1, leucin-rich repeat kinase 2 and α-synuclein. The validated transcripts are predicted to have non-coding functions and most of them were not annotated. Quantitative analysis of antisense transcripts in human tissues indicates enrichment in the brain, compatible with FANTOM 5 data. Overall, these results represent the most comprehensive analysis of antisense transcription at loci associated to neurodegeneration and provide evidence for the existence of additional regulation of disease-related genes by previously not-annotated long non-coding RNAs. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Zucchelli SIlvia, Paolo Vatta, Stefania Fedele, Raffaella Calligaris, XXXX (from F5 consortium), Al Forrest, Piero Carninci and Stefano Gustincich &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;SZ designed the experiments, analyzed the data, wrote the manuscript; PV performed the bioinformatics analysis, prepared some figures; SF designed the experiments, performed the experiments and analyzed the data; RC provided reagents, designed the experiments and analyzed the experiments; SG analyzed the data, wrote the manuscript &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on human brain and blood samples&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Research, Plos Genetics, Human Molecular Genetics&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: beginning of june&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:gustinci@sissa.it,silvia.zucchelli@sissa.it Stefano Gustincich, Silvia Zucchelli] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Zucchelli FANTOM5 Manuscript 2013 01 22.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;&amp;lt;br&amp;gt;[[Image:Zucchelli FANTOM5 Figures 2013 01 22.pdf]]&amp;lt;br&amp;gt; [[Image:Zucchelli FANTOM5 Supplementary 2013 01 22.pdf]]&amp;lt;br&amp;gt;[[Image:Zucchelli FANTOM5 TAbles 2013 01 22.pdf]] &lt;br /&gt;
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&lt;br /&gt;
== Title:Gateways to the promoter level mammalian expression atlas covering thousands of biological states in FANTOM5  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_025 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;working draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&amp;amp;nbsp;&#039;&#039;&#039;Monitoring RNA transcribed within a cell is an essential step toward the identification of active information within the genome, and the understanding the entire cellular system ultimately. Most previous studies involving the collection of a large set of genome-wide transcription profiles consist of tissues and/or cell lines. In the FANTOM5 (Functional ANnotation Of Mammals 5) project we monitored transcription in more than one thousand mammalian samples, including nearly two hundred primary cell types in human and more than one hundred cell types in mouse. We used a sequencing-based digital counting technology, CAGE (Cap Analysis Gene Expression), which skips any PCR amplification steps relying on a single molecule sequencer. &amp;amp;nbsp;This technology quantifies transcription starting site (TSS) activities at a single base pair resolution across the genomes, and the result is one of the largest sets of expression data available, consisting of diverse range of samples with a single platform based on the state-of-the-art technology. &lt;br /&gt;
&lt;br /&gt;
We assembled the FANTOM5 TSS profiles and subsequent analyses into a centralized data archive and set up various on-line resources available for the scientific community. Researchers in cell biology can easily search samples of interest to inspect active elements within a cell type. Researchers in molecular biology can search genes or transcription factors of interest to inspect in which biological context they are highly activated. Researchers in genome biology and other fields can explore the data within dynamic and interactive graphical user interfaces dedicated for genomic viewing and expression. We based all analysis and database systems on careful annotation of the diverse range of samples, including an application ontology consisting of cell types, anatomy, and diseases. This large set of expression data combined with the extensive and systematic sample annotation enables the scientific community to explore, examine, and slice the data from multiple aspects. Here we introduce the on-line resources and underlying data structure as well as discuss its potential impact in multiple research fields.&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;WP4, database providers, and analysis providers&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on phase1 freeze&amp;amp;nbsp;&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;package of word, pdf, etc: &#039;&#039;&#039;[[Image:130225-F5web-resource.zip]] &lt;br /&gt;
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== Title:Application of Semantic MediaWiki to snapshot of thousands of biological states in transcription  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_026 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Unknown&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;overview and instruction to the resource browser&#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: Shimoji H, Kawaji H., WP4 &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on phase1 freeze &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title:Identification of miRNA promoters and primary structures  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_028 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Unknown&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: ...&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: Kawaji H.&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Mogrify: Defining Factors For Direct Reprogramming Between All Cell Types  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_31 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft -&amp;amp;gt; PHASE2?&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
We now know that cellular state is a plastic phenomenon which it is possible to control. There are an increasing number of reports in the literature of induced pluripotency and also induced trans-differentiated from one cell type to another. Each of these experiments has relied heavily on a process of trial and error as well as expert knowledge in order to discover the transcription factors capable of inducing a cell conversion. Here we present a novel network based method (Mogrify) that can identify the factors required for cell conversion. The method compares differences in expression, as measured by FANTOM5 CAGE data, over interaction networks. It provides candidate combinations of transcription factors for over-expression and knock-down, along with the likelihood score for conversion between any two given cell types. &lt;br /&gt;
&lt;br /&gt;
We show that the method reproduces known reprogramming factors for several successful trans-differentiations from the literature (eg between fibroblast and cardiomyocyte, neuron and hepatocyte); we discuss alternative combinations that Mogrify suggests for these conversions and for other conversions which have some experimental data in the literature but for which a fully successful differentiation is yet to be published. &lt;br /&gt;
&lt;br /&gt;
The technique is then run without human intervention on every possible pairwise combination of over 1000 libraries in the FANTOM 5 set, assessing possible combinations of factors for perturbation, and associating a likelihood score for success. This information is then used to construct a computational “Waddington landscape”, identifying the best candidate source and target cell types for future cell conversion experiments. This is the first resource of it’s kind, only made possible by the new FANTOM5 promoterome data and represents a considerable step forward in computational cell reprogramming. &lt;br /&gt;
&lt;br /&gt;
.&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Owen and Julian &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks in all samples &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:owen.rackham@bristol.ac.uk,gough@cs.bris.ac.uk Owen Julian] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Mogrify.pdf]] &lt;br /&gt;
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== Title: Investigating tissue-specificity of cancer-causing mutations  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_037 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Over the past 10 years an increasing number of mutated genes have been associated with familial predisposition to cancer. Interestingly for more than half of these genes their involvement in cancer is restricted to only a few cancer types (e.g. BRCA1 mutations in breast and ovarian cancers). Even more interestingly some of these genes are expressed in all cell types, and perhaps we would expect to see them causing many more different types of cancer but they don’t. This paper will examine how these mutations are tolerated in most cell types but not in others by considering the network of genes expressed in different cell types and how that determines whether they are susceptible or resistant. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Jessica Mar, Daniel Carbajo, RIKEN_OSC_members, Alistair Forrest &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;JM and AF conceived the project, DC conducted the analyses. &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:jessica.mar@einstein.yu.edu Jessica Mar] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title:FANTOM5 reveals the genomic architecture of the genes implicated in Rett Syndrome  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_038 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Manuscript&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; Mutations in MECP2, FOXG1 and CDKL5 genes cause Rett Syndrome, a neuro-developmental disorder of the grey matter of the brain that almost exclusively affects females. We analyzed the RNA expression data from the FANTOM5 project in both human and mouse to investigate the genomic architecture of the three genes involved in Rett syndrome. Data from FANTOM 5 provides the unprecedented opportunity to study the expression profile, identify transcription start sites and, in conjunction with the recently released ENCODE dataset, identify the regulatory regions and transcription regulators of the three genes implicated in Rett Syndrome. Even though MECP2 and CDKL5 are expressed ubiquitously, mutations in these genes cause a brain specific phenotype suggesting that their role in brain is distinctly important from their function in other tissues. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors:&#039;&#039;&#039; Morana Vitezic, Leonard Lipovitch, Alistair RR Forrest, Piero Carninci, Alka Saxena &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; NAR &amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; December 2012 &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:mvitezic@gmail.com,alka@gsc.riken.jp Morana Vitezic Alka Saxena] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Rett paper.doc]] [[Image:Rett paper figures.zip]] [[Image:Rett paper supplementary.zip]]&amp;lt;br&amp;gt;&lt;br /&gt;
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== Title: Tissue gene expression profiles in relationship to primary cell gene expression profiles  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_039&amp;lt;br&amp;gt; &#039;&#039;&#039;Status:&#039;&#039;&#039; Initiated&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; Gene expression profile in a particular tissue determines the functionalities and signature properties in contrast with other tissues within the same organism. It is uncertain whether gene expression profiles in tissues are simply the results of a combination of gene expressions of the group of constituting primary cells, or if gene expression profiles differ when primary cells have been isolated from the tissues. In this paper, we would like to investigate the gene expression profiles of primary cells in relationship to tissue expression profiles. We are interested in finding out what kind of genes are involved in the differences and what functions they might have. We aim to find out to what degree do tissues resemble the sum expression of its composing cells, and if there are genes that are expressed in a tissue environment only.&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Nancy Yu, Carsten Daub, possibly members from the Human Protein Atlas (HPA) group. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement:&#039;&#039;&#039; NY will plan, perform most of the bioinformatics analyses and write the manuscript. CD will supervise the bioinformatics analysis, contribute additional ideas, and assist with manuscript writing. The HPA group will supply some data and possibly contribute to the bioinformatics analyses. &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used:&#039;&#039;&#039; Phase1 CAGE peaks and possibly HPA RNA-Seq data&amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s):&#039;&#039;&#039; Genome Research / PLoS Genetics / Genome Biology &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date:&#039;&#039;&#039; 2014 &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email:&#039;&#039;&#039; [mailto:nancy.yu@ki.se,carsten.daub@ki.se Nancy Yu, Carsten Daub] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors:&#039;&#039;&#039; [[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt; &#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF):&#039;&#039;&#039; [[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title:Pan Cancer Biomarkers and Disruption of Gene Regulatory Networks in Cancer.  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_41 &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039;CAGE FANTOM5 data collection of cancer cell lines and corresponding primary cells enables us to study the changes in transcription and gene regulation that occur in cancer and drive its development. CAGE is a 5’ sequence tag technology and provides us with a snapshot of genome-wide transcription start sites and shows in unbiased way which parts of genome are being actively transcribed into RNA in any given biological state. We analysed the CAGE data from 123 cell lines representing 12 different cancer types and compared them to the corresponding normal/primary cells (141 samples). We show the protein coding genes and non-coding RNAs that are up-regulated or down-regulated across multiple cancer types and therefore are candidates for pan cancer biomarkers. Furthermore, we show the changes in transcription factor activities and enhancer usage in cancers as well as disruption in gene co-regulation. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039;  Bogumil Kaczkowski, the FANTOM5 consortium and Alistair Forrest&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;  &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:forrest@gsc.riken.jp] &lt;br /&gt;
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== Title: Pathogen specific monocyte transcriptional responses  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_008 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Wells &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:c.wells@uq.edu.au,a.beckhouse@uq.edu.au Christine Wells, Anthony Beckhouse] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Promoter specificity in transcription determines cell lineage choice  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_018 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Delayed (as of September 12th)&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;This paper will use pathprint (pathway fingerprinting) to develop an overall phylogenetic tree of all samples in F5 freeze1. This tree will be used to determine relative ancestry of samples and cluster them accordingly. SwitchEngine will be run to find switching in TSS at key junctions in differentiation. Will show TSS dynamics at these informative sites is associated with lineage-commitment. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Emmanuel Dimont, Gabriel Altschuler, Winston Hide&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;ED did ..., GA did ..., WH did ...&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on all of F5freeze1 &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:edimont@hsph.harvard.edu,gabrielaltschuler@googlemail.com,whide@hsph.harvard.edu Winston Hide, Emmanuel Dimont, Gabriel Altschuler]&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Gene duplication and promoter divergence in mammals.  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_020&amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Delayed&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Lukasz Huminiecki and Core RIKEN Authors &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... and LH did everything else&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ..., F5 promoter and enhancer datasets, TreeFam8&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Research&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: September 1st&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Lukasz.Huminiecki@ki.se Lukasz Huminiecki] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
&lt;br /&gt;
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== Title: Gene duplication and TF/miRNA regulatory network evolution in mammals.  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_021 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Delayed&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Lukasz Huminiecki and Core RIKEN Authors &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... and LH did everything else&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ... TreeFam8, miRBase, microRNA target predictions&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Research&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: December 1st&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Lukasz.Huminiecki@ki.se Lukasz Huminiecki] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Higher order chromatin structure and promoter activity  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_023 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Delayed -&amp;amp;gt; moved to PHASE2 &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Semple CA, Prendergast JG, et al &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: October 2012&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Colin.Semple@igmm.ed.ac.uk,prenderj@gmail.com Colin Semple, James Prendergast] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title:Building context depending TSS regions from thousands of profiles  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_024 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Unknown&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;about DPI &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Kawaji H, et al. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on phase1 freeze &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
&lt;br /&gt;
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== Title: Quantifying the informational complexity of transcriptional regulatory programmes  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_015 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;On-hold. Focussing on the biological results Phase1_016 rather than methods. Hope to return to methods later (phase2).&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; The regulation of gene expression defines cellular identity, it is the basis for organism development and it underlies many cellular responses to the environment. Its disruption is implicated in many diseases and changes in gene regulation appear to underlie many adaptations evident between species. Previously, genes have been grouped and interpreted based on their specificity of expression, for example house-keeping genes that are expressed by all cells in all conditions versus highly tissue restricted genes expressed by only one cell type at a particular developmental time. Although such studies have been informative they fail to capture important aspects of how a gene is regulated or account for the heterogeneous relatedness of samples. The expression pattern of a gene is the output of a regulatory program within the cell. A program that must affect many state changes (on, off, up, down) is likely to require more regulatory information (Kolmogorov complexity) than a program effecting fewer state switches. If we can quantify this &amp;quot;regulatory complexity&amp;quot; we can then start to address deeper questions as to where that regulatory information is encoded, how malleable it is through evolution and how susceptible it is to perturbation by mutation. For example, a greater regulatory complexity could correspond to a higher concentration of cis-regulatory sequences around the gene or alternatively a single binding site for a transcription factor that is the output of an extensive intracellular signalling network. To address these questions we have explored a range of possible measures regulatory complexity including distance weighted entropies, diversity and richness scores. This leads us to introduce a novel measure of regulatory complexity (CR). It is implemented as a hierarchical Baysian model parametrised through MCMC. The CR method can be thought of as a relative measure of the number of gene expression state changes occurring over a tree relating all analysed samples. A by-product of this analysis is a probabilistic scoring of gene expression state switches between all analysed gene expression libaries. CR is weighted to account for the genome wide similarity of gene expression between samples but does not depend on the inference of a fixed underlying tree topology. &amp;lt;font color=&amp;quot;green&amp;quot;&amp;gt;Note - this is intended as essentially a methods paper, see Phase1_016 for the biological insights paper&amp;lt;/font&amp;gt; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Sarah Baker, Martin Taylor &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;SB developed and implemented methods and performed general analyses; MT conceived the project and oversaw implementation and performed some of the analysis&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on primary cells from human and mouse.&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Bioinformatics or Genome Research&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date:&#039;&#039;&#039; ETA July 2013 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:martin.tayor@igmm.ed.ac.uk,sarah.baker@igmm.ed.ac.uk Martin Taylor, Sarah Baker]&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Cis encoding of the master developmental regulatory programme  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_016 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft, starting dataset being regenerated to incorporate improved method&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; The regulation of gene expression defines cellular identity, it is the basis for organism development and it underlies many cellular responses to the environment. Its disruption is implicated in many diseases and changes in gene regulation appear to underlie many adaptations evident between species. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Sarah Baker, Martin Taylor &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;SB developed and implemented methods and performed general analyses; MT conceived the project and oversaw implementation and performed some of the analysis&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on primary cells from human and mouse. We may also want to use time course data for this paper (does that push it into phase2?).&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;PLoS Biology&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date:&#039;&#039;&#039; ETA March 2013 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:martin.tayor@igmm.ed.ac.uk,sarah.baker@igmm.ed.ac.uk Martin Taylor, Sarah Baker]&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Comparison of CAGE and RNA-Seq profiling results for human tissue and cell line data ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_042 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status:&#039;&#039;&#039; Initiated&amp;lt;br&amp;gt;&#039;&#039;&#039;Abstract:&#039;&#039;&#039; A systematic comparison of CAGE and HPA RNA-Seq tissue and perhaps cell line dataset, since both datasets will probably serve as widely used gene expression resources for the research community. This study will inform the researchers of the features of each dataset, including consensus and individual strengths of each data source. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039; Nancy Yu, Carsten Daub, possibly members from the Human Protein Atlas (HPA) group. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;NY will plan, perform most of the bioinformatics analyses and write the manuscript. CD will supervise the bioinformatics analysis, contribute additional ideas, and assist with manuscript writing. The HPA group will supply some data and possibly contribute to the bioinformatics analyses. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039; phase1 CAGE peaks, HPA RNA-Seq data &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; early 2014 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:nancy.yu@ki.se,carsten.daub@ki.se Nancy Yu, Carsten Daub] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title:CAGExploreR: an R package for the analysis and visualization of promoter dynamics across multiple experiments  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID&#039;&#039;&#039;&#039;&#039;: &#039;&#039;Phase1_043 &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;NOTE:&#039;&#039;&amp;amp;nbsp;This is a paper describing what used to be called &amp;quot;SwitchEngine&amp;quot;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;&#039;&#039;Status: &#039;&#039;&#039;Complete. Ready for Submission. &amp;lt;br&amp;gt;&#039;&#039;&#039;Abstract: &#039;&#039;&#039;Alternate promoter usage is an important molecular mechanism for generating RNA and protein diversity. Cap Analysis Gene Expression (CAGE) is a powerful approach for revealing the multiplicity of transcription start site (TSS) events across experiments and conditions. An understanding of the dynamics of TSS choice across these conditions requires both sensitive quantification and comparative visualization. We have developed CAGExploreR, an R package to detect and visualize changes in the utilization of specific TSS in wider promoter regions in the context of changes in overall gene expression when comparing different CAGE samples. These changes provide insight into the modification of transcript isoform gen-eration and associated regulatory network alterations associated with cell types and conditions. CAGExploreR is based on the FANTOM5 and MPromDb promoter set definitions but can also work with user-supplied regions. The package compares multiple CAGE libraries simultaneously and does not require replicates. Online supplementary materials describe methods in detail and a vignette demonstrates a workflow with a real data example.&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Emmanuel Dimont, Alistair R. R. Forrest, Hideya Kawaji, Winston Hide and the&amp;amp;nbsp;FANTOM Consortium&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;ED developed the method, the R package (software), wrote the paper and supplementary materials plus figures, AF created the original idea and provided data, HK created DPI TSS&amp;amp;nbsp;clusters (promoters), WH formulated the idea, wrote the paper and provided funding, FC provided funding and data.&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 DPI clusters, ENCODE CAGE data for MCF7 and A549 cell lines&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Bioinformatics&amp;amp;nbsp;(Application Note)&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;October 7th, 2013&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;Emmanuel Dimont (edimont@mail.harvard.edu)&amp;amp;nbsp;&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;The latest version of the manuscript, supplementary methods, R&amp;amp;nbsp;package and vignette can be found at [https://www.dropbox.com/sh/h9bf81ia56ywskq/gMPZ2KVfmi here].&amp;amp;nbsp;&amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;see above&#039;&#039;&#039;&amp;amp;nbsp;&#039;&#039;&#039; &lt;br /&gt;
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== Title:COPY THEN EDIT THIS TEMPLATE  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_00x (INCREMENT THIS) &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: ...&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: R&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:blah@change.this.edu,next.adress@change.this CHANGETHIScorresponding1 CHANGETHIScorresponding2] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_submission&amp;diff=7054</id>
		<title>Satellite submission</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_submission&amp;diff=7054"/>
		<updated>2013-11-05T12:37:55Z</updated>

		<summary type="html">&lt;p&gt;Yulia: /* Title: Effect of cytosine methylation on transcription factor binding sites and regulation of transcription */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;== Satellite manuscript internal review page  ==&lt;br /&gt;
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Welcome to the FANTOM5 Satellite review page. As discussed at the Ume and Koyo meetings, all papers will be visible to consortium members. This is to allow everyone to know what is going on, promote collaboration, carry out due process regarding co-authorship and to avoid competition. &lt;br /&gt;
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== Authorship  ==&lt;br /&gt;
&lt;br /&gt;
The author list will basically be selected by the first author and the corresponding author of each satellite paper on the basis of the scientific contribution to the manuscript. Remember to include an authors contribution statement for all authors named in your manuscript (of the form AB carried out the cell isolation, SB carried out the network predictions etc.). &lt;br /&gt;
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In addition the FANTOM5 headquarter will name RIKEN OSC members who should be co-authors for their input on each manuscript and to the entire FANTOM5 project. For those of you who have participated in previous FANTOMs you will be familiar with this process, for those new to FANTOM please look at the author lists on the satellite paper collections for FANTOM2-4. FANTOM5 headquarter is currently discussing the policy for RIKEN OSC co-authorship on the FANTOM5 satellites, but basically satellites papers will be considered on a case by case basis, and will take into account datasets used, intellectual input and facilitating technologies/analyses for each paper. &lt;br /&gt;
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At this stage please name any authors from the OSC that you think should definitely be included as co-authors, in addition for all satellite submissions include the following term &#039;&#039;&#039;RIKEN_OSC_members&#039;&#039;&#039; as an additional author. &lt;br /&gt;
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== Instructions  ==&lt;br /&gt;
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Please make a copy of the template below and enter your manuscript details. &lt;br /&gt;
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If you are not able to edit the wiki yourself please email the secretariat with the subject line &amp;quot;FANTOM5_satellite&amp;quot;, but please understand that these will be processed when we can rather than immediately. You must fill in all of the details below and provide both a PDF that contains all figures, and word doc of the main text, for reviewers to mark up directly. &lt;br /&gt;
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== RIKEN affiliation and acknowledgements in Satellite papers - guidelines ==&lt;br /&gt;
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As of April 1st, 2013, Omics Science Center has ceased to exist as a part of RIKEN reorganization. Many OSC members have changed their affiliation to other RIKEN centers or institutions. Therefore there has been a change in the way affiliations and acknowledgements are written on the Phase 1 satellite papers.&lt;br /&gt;
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Please consult the below guidelines before submitting the paper. For the existing manuscripts/manuscripts under submission please change affiliations and acknowledgements accordingly.&lt;br /&gt;
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Also, authors should &#039;&#039;&#039;send the manuscripts to &#039;&#039;&#039;[mailto:fantom5-secretariat@gsc.riken.jp FANTOM5 Secretariat] for checks before submitting the paper or the final proof to avoid trouble later.&lt;br /&gt;
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Guidelines: [[File: F5_affiliation_acknowledgements_130816.pdf]]&lt;br /&gt;
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= Manuscripts  =&lt;br /&gt;
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== Title: Epigenetic factors regulating Hematopoiesis  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_004 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;The hematopoietic differentiation pathway is a complex regulatory program for generating different lineages of blood cell types from multipotent, hematopoietic stem cells. The transcriptional program dictating hematopoietic cell fate and differentiation requires an epigenetic memory function consisting of a network of enzymes controlling DNA methylation, histone posttranslational modifications and chromatin structure. Defective interactions between epigenetic enzymes and transcription factors cause perturbations in blood cell differentiation, which often leads to various types of hematopoietic disorders such as leukemia. To elucidate the contribution of different epigenetic factors in human hematopoieis, high-throughput Cap Analysis of Gene Expression (CAGE) sequencing was used to build comprehensive transcription profiles of 199 epigenetic factors in a wide range of blood cells. These epigenetic factors include proteins that covalently modify DNA/histones or alter chromatin structure dynamics. Our analysis revealed several epigenetic factors to have expression profiles specific for cell type, lineage type and/or leukemic cell lines. In this report the ‘epigenetic transcriptome’ has been systematically studied to predict their potential functions in the epigenetic regulatory network of human hematopoiesis. The potential of such a comprehensive study is not only to identify putative epigenetic regulators of normal hematopoiesis and postulate their function but also to serve as a resource for the scientific community for further characterization and validation of differentially expressed transcripts. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Punit Prasad, Michelle Rönnerblad,...FANTOM5, Erik Arner, Karl Ekwall and Andreas Lennartsson &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;PP and MR have done analysis and written the manuscript. EA has performed the initial CAGE analysis for the epigenetic factors and assisted in writing the manuscript. AL and KE have assisted in writing the manuscript, planned and coordinated the study. The authors declare no conflict of interest.&amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ... &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Blood or other&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;December 06, 2012&amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:andreas.lennartsson@ki.se,arner@gsc.riken.jp Andreas Lennartsson, Erik Arner] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Prasad et al Blood 020213 .docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Prasad et al Blood 020213 .pdf]] &lt;br /&gt;
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== Title: Redefinition of the human mast cell transcriptome by deep-CAGE sequencing ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_009 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;Despite their haematopoietic origin, mast cells (MCs) mature exclusively in peripheral tissues, hampering research into their developmental and functional programs. Here, we employed deep-CAGE on skin-derived MCs to generate the most comprehensive view of the human MC transcriptome ever reported. A particular advantage is that MCs were embedded in the FANTOM5 project, giving the opportunity to contrast their molecular signature against an extensive panel of human samples. We demonstrate that MCs possess a unique and surprising transcriptional landscape, combining expression of typical haematopoietic genes with those exclusively active in MCs, and genes not previously reported as expressed in MCs. Specifically we found that MCs express functional BMP receptors, which transduce pro-survival and activatory signals. Conversely, several genes frequently studied in MCs were either not or only weakly expressed in direct comparison with other myelocytes. By the parallel use of MCs ex vivo and following culture, we also found that MCs change their transcriptome in in vitro surroundings. Befitting their uniqueness, MCs had no close relative in the haematopoietic network. This rich dataset reveals that our knowledge of human MCs is still fairly limited. It can be anticipated that with this resource novel functional programs of MCs will soon be discovered.&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Efthymios Motakis,1,* Sven Guhl,2,* Yuri Ishizu,1 RIKEN OSC members,1 Torsten Zuberbier,2 Alistair R R Forrest,1¶ Magda Babina2¶&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;E.M. carried out bioifnormatics analayses S.G. isolated the mast cells and performed most experiments, M.B. performed several experiments, was involved in planning, supervision, and data analysis, and wrote the first draft of the manuscript, E.M. S.G., A.R.R.F. and T.Z. helped with planning, data analysis and manuscript writing. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on mast cell samples in comparison to freeze 1 data &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Blood, eBlood &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:magda.babina@charite.de,sven.guhl@charite.de Magda Babina, Sven Guhl] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:BLOOD-2013-483792v1-Forrest.pdf]] &lt;br /&gt;
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== Title: Transcription and enhancer profiling in human monocyte subsets  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_011 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Human blood monocytes comprise at least three subpopulations that differ in phenotype and function. Here we present the first in-depth regulome analysis of classical (CD14++CD16-), intermediate (CD14+CD16+), and nonclassical (CD14dimCD16+) monocytes. Cap Analysis of Gene Expression (CAGE) adapted to Helicos single molecule sequencing was used to map transcription start sites throughout the genome in all three subsets. In addition, global maps of H3K4me1 and H3K27ac deposition were generated for classical and nonclassical monocytes defining enhanceosomes of the two major subsets. We identify differential regulatory elements (including promoters and putative enhancers) that were associated with subset-specific motif signatures corresponding to different transcription factor activities and exemplarily validate a novel downstream enhancer of the CD14 locus. In addition to known subset specific features, pathway analysis revealed marked differences in metabolic gene signatures. While classical monocytes expressed higher levels of genes involved in carbohydrate metabolism priming them for anaerobic energy production, nonclassical monocytes expressed higher levels of oxidative pathway components and showed a higher routine mitochondrial activity. Our findings describe promoter/enhancer landscapes and provide novel insights into the specific biology of human monocyte subsets. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Christian Schmidl, Kathrin Renner, Ruediger Eder, Katrin Peter, Petra Hoffmann, Reinhard Andreesen, Marina P. Kreutz, RIKEN_OSC_members, Matthias Edinger, Michael Rehli &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;CS performed experiments, computational analyses and wrote parts of the manuscript writing, KR performed experiments and contributed to manuscript writing, RE isolated the cells, KP performed experiments, PH, RA, MK, and ME contributed to planning and supervision, RIKEN_OSC_members who organized or performed Helicos sequencing and provided aligned data; MR initiated, planned and supervised the study, performed computational analyses, and wrote the manuscript. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on monocyte subsets (Regensburg samples) &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Blood, eBlood, other &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: September 1 ,2012 &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:michael.rehli@ukr.de,Christian.Schmidl@klinik.uni-regensburg.de Michael Rehli, Christian Schmidl] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Schmidl MonoSub.docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Schmidl MonoSub.pdf]]&amp;amp;nbsp;&amp;amp;nbsp; &lt;br /&gt;
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== Title:The enhancer and promoter landscape of regulatory and conventional T cell subpopulations  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_34&amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; CD4+CD25+FOXP3+ human regulatory T cells (Treg) are essential for self-tolerance and immune homeostasis. Here, we describe the promoterome of CD4+CD25highCD45RA+ naïve and CD4+CD25highCD45RA– memory Treg and their CD25– conventional T cell (Tconv) counterparts both before and after in vitro expansion by cap analysis of gene expression adapted to single molecule sequencing (HeliscopeCAGE). We performed comprehensive comparative digital gene expression analyses and revealed new orphan transcription start sites, of which several were validated as alternative promoters of known genes including FOXP3 and CTLA4. For all in vitro expanded subsets, we additionally generated genome-wide maps of poised and active enhancer elements marked by histone H3 lysine 4 monomethylation and histone H3 lysine 27 acetylation. Analysis of cell type-specific regulatory elements revealed a specific enrichment of several transcription factor binding motifs. We validated promising candidates by chromatin immunoprecipitation coupled to next generation sequencing and identified STAT5 and FOXP3 as well as RUNX1 and ETS1 as global regulators of Treg- and Tconv-specific enhancers, respectively. In summary we provide a highly detailed and easily accessible resource of gene expression and -regulation in Treg and Tconv subpopulations. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: R&#039;&#039;&#039; &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Blood&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:christian.schmidl@klinik.uni-regensburg.de,michael.rehli@klinik.uni-regensburg.de Christian Schmidl, Michael Rehli] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:121027 FANTOM Treg manuscript.docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Schmidl Treg.pdf]] &lt;br /&gt;
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== Title: Effect of cytosine methylation on transcription factor binding sites and regulation of transcription  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_010 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BMC GENOMICS&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Background: DNA methylation in promoters is strongly linked to downstream gene repression. However, the question remains as to whether DNA methylation is a cause or a consequence of gene repression. In the former case, DNA methylation may affect the affinity of transcription factors (TFs) towards their binding sites (TFBSs). In the latter case, gene repression caused by chromatin modification is stabilized by DNA methylation. Until now, the above-mentioned scenarios have been only supported only by non-systematic evidences and have not been tested for a wide spectrum of TFs. Although the average promoter methylation is usually used in related studies, recent results suggested that methylation of individual cytosines can be also important. &amp;lt;br&amp;gt; Results: We found that for 16.6% of cytosines methylation profile and the expression profile of neighboring TSSs were significantly anti-correlated. We named CpG corresponding to such cytosines as “traffic lights”. We observed a strong selection against CpG “traffic lights” within TFBSs. The negative selection was stronger for transcriptional repressors as compared to transcriptional activators or multifunctional TFs as well as for core TFBS positions as compared to flanking TFBS position.&amp;lt;br&amp;gt; Conclusions: Our results indicate that direct and selective methylation of certain TFBS that prevents TF binding is restricted to only special cases and cannot be considered as a general regulatory mechanism of transcription.&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Yulia A Medvedeva, Abdullah Khamis, Ivan V Kulakovskiy, Wail Ba-Alawi, Md Shariful I Bhuyan, Hideya Kawaji, Timo Lassmann, Matthias Herbers, Alistair RR Forrest, Vladimir B Bajic and the FANTOM consortium&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;YAM designed the computational experiments, selected and preprocessed the data, produced statistical analysis and wrote the manuscript; AK performed most of the data analysis; WBA and MdSIB contributed RDM models and tools for threshold estimation and mapping; [potential F5 collaborators], IVK performed part of the analysis, contributed to the design of the experiments and writing of the manuscript; VBB contributed to the design of the experiments and writing of the manuscript. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on 50 sample types, ENCODE RRBS data for the same samples &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Genome biology&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;December, 16 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:ju.medvedeva@gmail.com Yulia Medvedeva] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Effect of cytosine methylation on transcription factor binding sites and regulation of transcription.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Effect of cytosine methylation on transcription factor binding sites and regulation of transcription.pdf]] &amp;lt;br&amp;gt;&#039;&#039;&#039;Additional files for general viewing: &#039;&#039;&#039;[[Image:Effect of cytosine methylation on transcription factor binding sites Additional files.zip]] &amp;lt;br&amp;gt; &amp;quot;&amp;quot;Accepted version: &amp;quot;&amp;quot; [[Image:Medvedeva et al_ accepted.zip]]&lt;br /&gt;
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== Title: The Evolution of Human Cells in terms of Protein Innovation  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_013 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT MOLECULAR BIOLOGY AND EVOLUTION&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Humans are complex organisms composed of a great many cell types. Since the genomic DNA of each cell is identical, cell type is determined by what is expressed. We examine the evolutionary history of each human cell type at the molecular level via the collective histories of proteins, the principal product of gene expression. Sequence data from the FANTOM5 consortium are used to provide cell-type specific digital expression of protein-coding genes, and the SUPERFAMILY and dcGO resources provide domain and function annotation respectively. Cross-referencing with the domain annotation of all other completely-sequenced genomes provides the evolutionary context for each protein. We combine all of this to generate a description of cellular evolution at the molecular level. &lt;br /&gt;
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We present a protein domain view of the evolution of cell type. To achieve this we first identify the most recent common ancestor (MRCA) or ‘creation epoch’ of every protein in the repertoire of the human genome. We are then able to use the protein creation epochs to describe the history of the emergence of each cell type over evolution in terms of the collective histories of the proteins expressed in that cell type. Each cell type has an evolutionary profile consisting of a timeline along the lineage from the ancient cellular ancestor to modern day human. The profile of each cell type shows at which epochs along the timeline innovations in protein evolution took place; required to allow the observed expression in that type of cell. By clustering cell types on these profiles, we find groups of cell types that share a parallel protein evolutionary history and thus potentially possess a common progenitor cell type or are evolving in cooperation. A functional enrichment analysis of these clusters reveals key proteins responsible for evolutionary shifts and functional innovations; it also suggests a possible order in which different cells could have emerged during evolution, which we discuss in relation to the human immune system. The structural domain-centric perspective which we employ in this work can also be used as the basis for a comparison of the molecular basis of functional and phenotypic differences between cell types within these evolutionary clusters, exemplified by an inspection of our results on different regions of the brain. &lt;br /&gt;
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We present a view of the landscape of nature’s innovation of protein structure and architecture required to explain the creation of the different human cell types. This landscape has some important features such as the possibility that the last universal ancestor of life provided most of the innovation for the innate immune system whilst brain cells have been making use of novel proteins that first appeared in opisthokonta (animals and fungi) and continued to do so right up until homo sapiens. The landscape also lends itself to identifying candidate genes for disease by highlighting those that were important in enabling certain phenotypic shifts at key points in evolution.&amp;lt;br&amp;gt; &lt;br /&gt;
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Authors: &#039;&#039;&#039;Adam J. Sardar, Matt E. Oates, Hai Fang, Alistair R.R. Forrest,Hideya Kawaji, Julian Gough, Owen J.L. Rackham and the FANTOM Consortium&#039;&#039;&#039; &lt;br /&gt;
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Authors contribution statement: FANTOM5 was made possible by a Research Grant for RIKEN Omics Science Center from MEXT to Yoshihide Hayashizaki and a Grant of the Innovative Cell Biology by Innovative Technology (Cell Innovation Program) from the MEXT, Japan to Y.H.. We would like to thank all members of the FANTOM5 consortium for contributing to generation of samples and analysis of the dataset and thank GeNAS for data production. A.J.S. and M.E.O. were funded by BCCS studentships from EPSRC [EP/E501214]; another funding source was the BBSRC [BB/ G022771/1 to J.G., funding O.J.L.R. and H.F.].The authors would like to thank David de Lima Morais for useful discussion at the preliminary stages of this work. &amp;lt;br&amp;gt; Datasets used: &#039;&#039;&#039;Helicos CAGE on all samples &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s):&#039;&#039;&#039;GR&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:gough@compsci.bristol.ac.uk,owen.rackham@gmail.com Julian Gough, Owen Rackham] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Rough draft available on request]] &amp;lt;br&amp;gt; &#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): submitted revisions: [[Full_Manuscript_Sardar_et_al.pdf‎]] &#039;&#039;&#039;[[Image:TraP Journal Submission.zip]]&#039;&#039;&#039; [[Image:GR Submission 3 March Sardar 2013 The Evolution of Human Cells in terms of Protein Innovation.pdf]] &lt;br /&gt;
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== Title:Comparison of CAGE and RNA-seq transcriptome profiling using a clonally amplified and single molecule next generation sequencing  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_027 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT GENOME RESEARCH&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; CAGE (Cap Analysis Gene Expression) and RNA-seq are two major technologies used for transcript quantification. These protocols measure expression by from either the 5’ end of capped molecules (CAGE) or tags randomly distributed along the length of a transcript (RNA-seq). Library protocols for clonally amplified (Illumina, SOLiD, 454, Ion Torrent) 2nd generation sequencing platforms typically employ PCR pre-amplification prior to clonal amplification, while 3rd generation single molecule sequencers can sequence unamplified libraries. While these protocols individually have been demonstrated to be highly reproducible, no systematic comparison has been carried out between the protocols. Here we compare CAGE using both 2nd and 3rd generation sequencers and RNA-seq using a 2nd generation sequencer based on a panel of RNA mixtures from two human cell lines (THP-1 and HeLa, 100%, 50%, 20%, 10%, 5%, 1% and 0% of HeLa RNAs) to examine power to discriminate biological states, to detect differentially expressed genes, linearity of measurements as well as quantification reproducibility. Quantification by CAGE with the 2nd and 3rd generation sequencers (Illumina GA-IIx and HeliScope) were consistent at gene level, however we observed several differences, which can be explained by differences in their protocols and sequencing platforms. These include significant bias in the Illumina library, such as GC biases and over-estimation of transcripts harboring internal Ecop15I sites., A poorer correlation at the level of individual TSS positions, which is likely to be due to higher indel rate in HeliScope, is also found. We found high consistency between HeliScopeCAGE with RNA-seq (spearman correlations 0.88). Differences between CAGE and RNA-seq are explained by incompleteness of existing gene models in most cases, where 5’-ends of gene models do not reflect actual transcription starting site in the profiled cells, or RNA polymerase run through the poy adenylation site resulting in fusion of neighboring genes. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;WP3 &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;Genome Res. &#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: 23rd Dec, 2012 &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Submitted PDF: &#039;&#039;&#039;[[Image:130215-PlatformEval-submittedGR.pdf]]  &lt;br /&gt;
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== Title: Differential roles of epigenetic conversion and Foxp3 expression in regulatory T cell-specific transcriptional regulation  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_029 &amp;lt;br&amp;gt; &lt;br /&gt;
&#039;&#039;&#039;Status: ACCEPTED AT PNAS&#039;&#039;&#039;&amp;lt;br&amp;gt;&lt;br /&gt;
&#039;&#039;&#039;Abstract: &#039;&#039;&#039;Naturally occurring regulatory T (Treg) cells are engaged in the maintenance of immune tolerance and homeostasis. The development of Treg cells requires both the expression of the transcription factor Foxp3 and the establishment of Treg cell-type DNA hypomethylation pattern. By transcriptional start site (TSS) cluster analysis, we here assessed possible correlation of genome-wide DNA methylation pattern or Foxp3-binding pattern with Treg-specific gene expression. We found that Treg cell-specific DNA hypomethylated regions were closely correlated with Treg-upregualted TSS clusters, whereas Foxp3-binding regions had no significant correlation with either up- or down-regulated clusters, in non-activated Treg cells. On the other hand, in activated Treg cells, Foxp3-binding regions showed a strong correlation with down-regulated clusters. In silico search for transcription factor-binding motifs revealed that the motifs enriched in Foxp3-binding or Treg-specific DNA hypomethylated regions were mostly different. These results collectively indicate that Treg cell-specific DNA hypomethylation is conducive to up-regulation in the steady state Treg cells whereas Foxp3 expression to down-regulation of its target genes in activated Treg cells. Thus, the combination of the two events is required for the establishment of Treg cell-specific gene expression and function. &lt;br /&gt;
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(185 words)&amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Authors: &#039;&#039;&#039;Hiromasa Morikawa1,2, Naganari Ohkura1, Alexis Vandenbon3, RIKEN_OSC_members 4, Daron Standley3, Hiroshi Date2, Shimon Sakaguchi1 &lt;br /&gt;
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1. Department of Experimental Immunology, World Premier International Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan&amp;lt;br&amp;gt;2. Department of Thoracic Surgery, Kyoto University, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan&amp;lt;br&amp;gt;3. Department of Systems Immunology, World Premier International Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan&amp;lt;br&amp;gt;4. RIKEN Omics Center, Yokohama, Japan&amp;lt;br&amp;gt;&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &amp;amp;nbsp;Genome Research&#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &amp;amp;nbsp;2012/12/18&#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:hmorikawa@ifrec.osaka-u.ac.jp Hiromasa Morikawa] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: [https://fantom5-collaboration.gsc.riken.jp/wiki/index.php/File:Submit130114v3.docx Submit130114v3.docx]&#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF):&amp;amp;nbsp;[https://fantom5-collaboration.gsc.riken.jp/wiki/index.php/File:Submit130114v3.pdf Submit130114v3.pdf]&#039;&#039; &lt;br /&gt;
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== Title: An atlas of active enhancers across human cell types and tissues  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_35 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT NATURE&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; In higher organisms, cellular development and diversity is highly controlled by enhancers, which regulate the correct temporal and cell type-specific activation of gene expression. Despite their obvious importance for development and disease, the exact locations, target genes and mechanisms of enhancers are still poorly defined. Thus, there is an urgent need not only to identify enhancer locations, but also to elucidate their specific usage across the wide diversity of cells within the human body, their impact on regulation in healthy and diseased individuals, and how enhancers interact with target genes. Here, we use the FANTOM5 panel of tissue and primary cell samples covering the majority of human tissues and cell types to define an atlas of active, in vivo bidirectionally transcribed enhancers across the human body. It enables comparison of regulatory programs between different cells and tissues at unprecedented depth, and makes it possible to define distinct subsets of enhancers, including fetal-specific, cell-specific and ubiquitous enhancers – a novel enhancer subtype with distinct properties. We show that known target genes of enhancers can be recaptured using expression correlations and predict many novel enhancer-TSS associations. We present models confirming the utility of multiple redundant enhancers, which explain TSS expression strength rather than expression patterns. We demonstrate that disease-associated functional single nucleotide polymorphisms are over-represented in enhancers and that such enhancers often have disease-relevant expression patterns. The human enhancer atlas can be accessed through an online database and is a unique resource for studies on tissue/cell-specific enhancers and their gene interactions. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Robin Andersson1#, Claudia Gebhard2#, Irene Miguel-Escalada3, Ilka Hoof1, Xiaobei Zhao1, Christian Schmidl2, Eivind Valen1,4, Kang Li1, Lucia Schwarzfischer2, Dagmar Glatz2, Johanna Raithel2, Yun Chen1, Berit Lilje1, Nicolas Rapin1,5, Frederik Otzen Bagger1,5, Mette Jørgensen1, Mette Boyd1, Jette Bornholdt1, Kenneth Baillie6, Chris Mungall7, Timo Lassmann8, Hideya Kawaji8, Andreas Lennartsson9, Carsten Daub8,9, David Hume6, Peter Heutnik10, Alistair Forrest8, Piero Carninci8, Yoshihide Hayashizaki8, Ferenc Müller3, Michael Rehli2*, Albin Sandelin1* &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;RA, IH, EV, KL, YC, BL, XZ, MJ, HK, TL, KB, CM, NR, FOB, MR, AS made the computational analysis. TL, HK, CD, AF, PC, YH prepared, mapped and analyzed CAGE libraries. RA, CG, IH, EV, FM, PC, AF, AK, MB, JBL, AL, CD, DH, PH MR, AS interpreted results. CG, CS, ME, MR made the blood cell ChIP experiments, methylation assays and in vitro blood cell validations. IME, FM made zebrafish in vivo validations and interpretations. RA, CG, IH, FM, MR, AS wrote the paper. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks and raw CAGE mapped data from human, internal ChIP and other validation data &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; To be decided &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[robin@binf.ku.dk, michael.rehli@klinik.uni-regensburg.de, albin@binf.ku.dk , Michael Rehli Albin Sandelin] &amp;lt;br&amp;gt; &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] [[Image:Enhancerome full.pdf]]&#039;&#039;&#039; &lt;br /&gt;
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== Title: Analysis of DNA methylation and transcription during granulopoiesis reveals timed methylation changes in low CpG areas and regulation of transcription factor expression and motif activity  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_001 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;In development epigenetic mechanisms such as DNA methylation have been suggested to provide cellular memory to maintain pluripotency but also stabilize cell fate decisions and direct lineage restriction. In this study we set out to characterize changes in DNA methylation levels and gene expression during granulopoiesis using four distinct cell populations ranging from the oligopotent common myeloid progenitor stage to terminally differentiated neutrophils. We found a general decrease of DNA methylation during granulopoiesis. Methylation levels appear to change at specific differentiation stages and correlate with changes in transcription and motif activity of key hematopoietic transcription factors. Differentially methylated sites (DMSs) are preferentially located in areas distal to CpG islands and shores and are overrepresented in potentially regulatory enhancer elements. Overall this study depicts in detail the epigenetic and transcriptional changes that occur during granulopoiesis and supports the role of DNA methylation as a regulatory mechanism in cell differentiation. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Michelle Rönnerblad, Tor Olofsson, Sören Lehmann, RIKEN_OSC_members, Karl Ekwall*, Erik Arnér* &amp;amp;amp; Andreas Lennartsson* &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did most of the practical experiments, the bioinfo analysis (except CAGE related) and most manuscript writing, TO isolated the cells from bone marrows, SL gave valuable input to the planning, analysis and critically reviewed the manuscript, KE planned and supervised the study and contributed to the manuscript writing , EA supervised the bioinformatic analysis and performed the ones related to CAGE and contributed to the manuscript writing, AL initiated, planned and supervised the study and contributed to the manuscript writing and did some experiments. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on granulo precursor populations &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Blood &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;April 7th 2012 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:andreas.lennartsson@ki.se,Karl.Ekwall@ki.se,arner@gsc.riken.jp andreas lennartsson, Karl Ekwall, Erik Arner] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Rönnerblad.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Rönnerblad Aprl07.pdf]] &lt;br /&gt;
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== Title: Ceruloplasmin is a Novel Adipokine Which is Overexpressed in Adipose Tissue of Obese Subjects and in Obesity-Associated Cancer Cells  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_32 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT PLOS ONE&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; Obesity confers an increased risk of developing specific cancer forms. Although the mechanisms are unclear, increased fat cell secretion of specific proteins (adipokines) may promote/facilitate development of malignant tumors in obesity by cross-talk between adipose tissues and the tissues prone to develop cancer among obese. This was investigated using expression data from human adipose tissue of obese and non-obese as well as from a large panel of human cancer cell lines and corresponding primary cells and tissues. We identified three previously described adipokines, SERPINE1, SERPINE2 and C3 sharing a common cognate receptor LRP1 which was expressed in all cancer cell lines associated with obesity. Expression and secretion of SERPINE1 and C3 were increased in obese adipose tissue and their plasma levels were elevated in obese subjects. We also identified genes enriched in obesity-associated cancer cells compared to cell lines and corresponding healthy tissues or primary cells. We found expression of ceruloplasmin to be the most enriched in obesity-associated cancer cells. This gene was also significantly up-regulated in adipose tissue of obese subjects. Ceruloplasmin is the body’s main copper carrier and is involved in angiogenesis. We demonstrated that ceruloplasmin was a novel adipokine and that obese adipose tissue contributed markedly (22%) to the total protein level. In summary, we have identified several adipokines, which can serve as endocrine signals facilitating growth of obesity-associated cancer tumors. These adipocyte signals are increased in obesity and may be important for development of cancer associated with excess body fat. &lt;br /&gt;
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&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Erik Arner, Alistair Forrest, Anna Ehrlund, Niklas Mejhert, [Additional RIKEN people?], Jurga Laurencikiene, Mikael Rydén, Peter Arner &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s):&#039;&#039;&#039; Cancer Research &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:arner@gsc.riken.jp Erik Arner] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Fat cells and cancer draft 120816 EA.docx]] [[Image:Figs 2012-08-15.ppt]]&amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039; &lt;br /&gt;
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== Title: Interactive visualization and analysis of large-scale NGS data-sets using ZENBU  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_33 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT NATURE BIOTECHNOLOGY&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039;The world of genome sciences has dramatically changed over the last 5 years. With the advent of next generation sequencers and RNA-expression sequencing, genome science is no longer the domain of a few elite centralized &amp;quot;genome centers&amp;quot; like in the early days of the field. The advance of next-generation sequencers has spurred an ever-growing body of tag-based data allowing the survey of chromatin states and transcriptome dynamics. Visualization of expression levels of genomic regions was achieved by displaying expression levels in various experimental conditions in dedicated tracks allowing investigators a direct comparison of their dynamics. Novel file formats and browser design have allowed for dealing efficiently with the depth of data produced by next-generation sequencer based technologies. Researchers need to interact within global collaborations and need easy ways to process, share and visualize their data in a secured manner prior to publication. To this end we have developed the ZENBU system. ZENBU is a web based system which is a social networking platform for secured data upload and data sharing with collaborators, a data processing system, and a visualization system. ZENBU provides the infrastructure for working with 100s of terrabytes of sequence data in the form of BAM sequence alignment files and genome annotation formats like BED and GFF, to efficiently cross-analyze these databsets using a Map-Reduce/autonomous-agent based parallel processing system, and provide fast efficient web services for user interfaces. The user interfaces for ZENBU is based on Web2.0 technologies in the form of a new expression-enhanced genome browser, and data manipulation interfaces for data upload, data processing, and data download. ZENBU currently contains the entire FANTOM 3/4/5 datasets, the entire ENCODE datasets, and much of the UCSC genome annotation data. ZENBU is planned to be a corner stone in the expanding global network of scientific sharing web systems.&amp;lt;br&amp;gt; &lt;br /&gt;
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&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Jessica Severin*, Marina Lizio, Jayson Harshbarger, Hideya Kawaji, Carsten Daub, The FANTOM5 consortium, Yoshihide Hayashizaki, Nicolas Bertin*, Alistair Forrest* &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement:&#039;&#039;&#039; &#039;&#039;JMS, ML, JH, HK, CD, YH, NB, AL&#039;&#039; &lt;br /&gt;
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*JMS, wrote the software/webservices. &lt;br /&gt;
*JMS, NB, planned the study. &lt;br /&gt;
*NB supervised the study. &lt;br /&gt;
*JMS, NB, contributed to the manuscript writing. &lt;br /&gt;
*JMS, NB, gave valuable input to the analysis in the manuscript. &lt;br /&gt;
*JMS, NB, critically reviewed the manuscript. &lt;br /&gt;
*&#039;&#039;[addition of any other, clearer or more precise statement is very welcome]&#039;&#039;&lt;br /&gt;
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&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s):&#039;&#039;&#039; Nature Biotech/Genome Research &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:severin@gsc.riken.jp,nbertin@gsc.riken.jp,forrest@gsc.riken.jp Jessica Severin, Nicolas Bertin, Alistair Forrest] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of the most up to date manuscript draft: &#039;&#039;&#039;[[Image:ZENBU manuscript.014 (1).docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Cell-type specificity and co-expression of regulatory polymorphisms associated with human disease  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_002 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO GENOME RESEARCH&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Our ability to use genetic associations with disease to develop better treatments has been limited by the difficulty of identifying a biological process, or cell type, on which to focus investigation. Most disease-associated polymorphisms do not lie within protein-coding genes, raising the possibility that variation in regulatory sequence plays a critical role in disease phenotypes. We have used genome-scale 5’RACE (CAGE) to identify the location and usage of transcription start sites in 864 human tissues, primary cells and cell lines, and show here that there is a strong enrichment for disease-associated variants within the sequence immediately adjacent to transcription start sites. Using the expression profiles of known variants associated with disease susceptibility, we identify experimentally-available cell types significantly associated with specific diseases and traits. The expression of genes known to be associated with particular diseases was positively correlated. Such co-expression was used to identify unreported candidate disease-associated regulatory regions within published genome-wide association studies (GWAS). The approach was validated by identifying candidate loci in a 2007 GWAS study that were subsequently validated in larger independent datasets These functional genomics approaches directly inform choices of model system and identify disease- and cell type-specific co-regulated networks for a wide range of common diseases. &lt;br /&gt;
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&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Baillie JK*, Haley CS, Schaefer U, Faulkner GJ, Freeman T, Brown JB, [others...], [Numerous RIKEN authors, order etc. TBC, at least including: Kawaji H, Forrest A, Carninci P]*, Hume DA* &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on Primary Cells &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Nature Genetics &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; ...&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:j.k.baillie@ed.ac.uk,david.hume@roslin.ed.ac.uk Kenneth Baillie, David Hume] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Ab Initio Prediction of Tissue-Specific Regulatory Modules in the FANTOM5 Project  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_005 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO GENOME RESEARCH&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;One of the major goals of the FANTOM5 project, the broadest TSS-based promoter-level expression atlas of transcriptional regulatory networks, is the identification of coding and non-coding, annotated and novel transcriptional units being transcribed in a cell-specific mode across the different biological states/samples. In this work we analyzed the FANTOM5 dataset using ScanAll, a newly developed software here described, to ab initio predict the presence of conserved elements in the genomic regions surrounding FANTOM5 promoters. Firstly we aimed at identifying motifs that were conserved in a subset of the selected genomic regions and that possibly corresponded to Transcription Factor Binding Sites (TFBS); we then expanded our analysis to pinpoint the existence of more complex, structured regulatory modules, that is groups of conserved motifs co-occurring in the aforementioned (co-expressed) regions within a fixed distance. We confirmed the sample-specificity of our output by showing that the majority of the obtained combinations of modules were able to divide the specimens into sample-specific groups, thus possibly explaining the peculiarities of regulatory events occurring in each tissue. Among these sites it was possible to confirm the presence of TFBS for known regulators already associated to those samples together with an additional and significant portion of motifs remaining unannotated, thus representing putative novel binding elements. In addition we were able to associate the presence of a significant portion of the identified motifs to distinct families of repeated elements, thus confirming a structural/functional feature of mammalian promoters that is currently emerging as one of the most peculiar regulatory aspects associated to mammalian phylogeny. Finally, we were able to identify previously uncharacterized aspects of the regulatory networks occurring in early-development samples thus confirming the significant advantage deriving from our modular approach. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Emiliano Dalla, Yari Ciani, Marco Zantoni, Alberto Policriti, Hideya Kawaji, Michiel J.L. de Hoon, Timo Lassmann, Alistair R.R. Forrest, Michael Rehli, Ivan Kulakovsky, Claudio Schneider, Silvano Piazza &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;ED conceived the project, developed part of the software, oversaw implementation, performed some of the analysis and most manuscript writing; YC implemented part of the software, performed some of the analysis and prepared some figures; MZ developed and implemented part of the software; AP developed part of the software and contributed to the manuscript writing; TL was responsible for tag mapping; HK managed the data handling; MR, IK and MJLdH were involved in motif assessment; ARRF was responsible for FANTOM5 management and concept; CS supervised the study; SP developed and implemented part of the software, carried out statistical tests and results interpretation and wrote parts of the manuscript. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on all of F5freeze1 &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;June 1st 2012; Update: December 21st 2012: Post Internal Review Update: January 28th 2012 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:emiliano.dalla@lncib.it Emiliano Dalla] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:FANTOM5 PromoteromeSatelliteLNCIB.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:FANTOM5 PromoteromeSatelliteLNCIB wFigures.pdf]] &lt;br /&gt;
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== Title: A high resolution spatial-temporal promoterome of the human brain (was Brain CAGE)  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_007 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO GENOME RESEARCH&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;The human brain is an extremely complex organ that governs our abilities for cognition, reasoning and emotions and is the control center for the body. Its morphology and functionality during development have been well studied, but the molecular mechanisms contributing to its function and maintenance later in life remain poorly understood. Complexity at the transcriptional level is likely to play a major role in defining its morphological and functional characteristics. To investigate this we used single molecule CAGE and created a high resolution atlas of transcription start sites for 15 anatomical regions of the human central nervous system, using post-mortem samples derived from infant and aged adult donors. On the transcriptional level brain is clearly distinguishable from other tissues even if we consider only non-coding genes or expression from genomic regions often described as genomic dark matter. Using these differences we identify a specific set of transcription start sites that characterizes the brain. We show extensive differences in transcription between infant and adult that in some cases can be linked to loci associated with major neurodegenerative diseases. The differential expression across distinct regions correlates well with developmentally and/or functionally related anatomical districts and is refelected by distinct networks of interacting transcription factors, a range of lncRNAs and novel transcripts co-expressed in a regionally biased manner. Overall we provide the scientific community with a powerful expression resource based on post-mortem tissue, particularly highlighting the contribution of non-coding RNAs to the transcriptional complexity of human central nervous system. &lt;br /&gt;
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&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Margherita Francescatto, Morana Vitezic, Patrizia Rizzu, Javier Simon-Sanchez, Robin Andersson, FANTOM5_RIKEN_OSC_members, Carsten O Daub, Albin Sandelin, MIchiel JL de Hoon, Piero Carninci, Alistair RR Forrest, Peter Heutink &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MF and MV did the analyses; MF, MV and PH wrote the manuscript, PR selected all samples, evaluated medical and pathological records and isolated RNA, JSS curated the list of disease loci, RA and AS provided the list of enhancers, ARRF, PC and PH designed the study ... &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on VUMC provided brain samples (adult and newborn); full list of samples presented in Supplementary Table 1&amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Genome Research &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Peter.Heutink@dzne.de,m.francescatto@vumc.nl,mvitezic@gsc.riken.jp Peter Heutink, Margherita Francescatto, Morana Vitezic] &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Final version: &#039;&#039;&#039;[[Image:Francescatto and Vitezic manuscript.pdf]] [[Image:Francescatto and Vitezic figures.pdf]] [[Image:Francescatto and Vitezic Supplementary Note.pdf]]&amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Chromatin states reveal functional associations for globally defined transcription start sites in four human cell lines  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_017&amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO BMC GENOMICS&#039;&#039;&#039; &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: Background: &#039;&#039;&#039;Deciphering the most common modes by which chromatin regulates transcription, and how this is related to cellular status and processes is an important task for improving our understanding of human cellular biology. The FANTOM5 and ENCODE projects represent two independent large scale efforts to map regulatory and transcriptional features to the human genome. Here we investigate chromatin features around a comprehensive set of transcription start sites in four cell lines by integrating data from these two projects. &#039;&#039;&#039;Results:&#039;&#039;&#039; Transcription start sites can be distinguished by chromatin states defined by specific combinations of both chromatin mark enrichment and the profile shapes of these chromatin marks. The observed patterns can be associated with cellular functions and processes, and they also show association with expression level, location relative to nearby genes, and CpG content. In particular we find a substantial number of repressed inter- and intra-genic transcription start sites enriched for active chromatin marks and Pol II, and these sites are strongly associated with immediate-early response processes and cell signaling. Associations between start sites with similar chromatin pattern are validated by significant correlations in their global expression profiles. &#039;&#039;&#039;Conclusions:&#039;&#039;&#039; The results confirm the link between chromatin state and cellular function, but they also show that the relationship between chromatin state and transcription is more subtle than previously appreciated. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Morten Rye, Geir Kjetil Sandve, Finn Drablos&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR, GKS and FD did data analysis and wrote the paper&amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE data, ENCODE chromatin ChIP-Seq and DNase HS data&amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Genome Biology &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;01.03.2013&amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:finn.drablos@ntnu.no,morten.rye@ntnu.no Finn Drablos,Morten Rye]&amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Internal submission draft FD GKS MBR 010313.docx]] &amp;lt;br&amp;gt; &#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Main figures 01032015.pdf]] &#039;&#039;&#039;Supplementary figures: &#039;&#039;&#039;[[Image:All supplem figs 01032013.pdf]] &lt;br /&gt;
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== Title: Evolution of expression patterns in human gene families illustrated by the FANTOM5-CAGE encyclopedia of transcription start sites.  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_019 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO BMC EVOLUTIONARY BIOLOGY&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &lt;br /&gt;
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Background Human gene families emerged through consecutive rounds of gene duplication. Here we apply the cutting-edge FANTOM5 single-nucleotide resolution atlas of transcription start sites from 1348 human and mouse libraries, to elucidate expression pattern evolution in animal gene families, with stress on comparison between human and mouse, and normal versus cancer cells. &lt;br /&gt;
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  Results  Broad over-view of FANTOM5 was obtained with intra-species and inter-species hierarchical clustering of human and mouse samples. In the follow-up, we dated gene duplications by phylogenetic timing, and investigated the rate of expression pattern divergence between duplicates, as well as the tissue-specificity of their expression. Finally, we defined the concept of phylo-expression signatures as strong associations between duplications of certain ages and expression samples in the FANTOM5 atlas. We show how phylo-expression signatures can be used to generate novel hypotheses on the nature of animal evolution, and discuss central nervous system and reproductive tract as two focused examples.   &lt;br /&gt;
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Conclusions A striking trend for young genes to be narrowly expressed was revealed. Several lines of evidence suggested that emergence of placental mammals was a unique period in the evolution of animal gene families and duplicates dating to that period have broader and more conserved expression patterns, with genes involved in chromatin assembly and epigenetic control driving the trend. A major strength of the FANTOM5 atlas is that it profiles normal tissues, primary cells, and cancer cell lines, and as expected, clustering of expression profiles showed a major divide between leukemias and solid tumors. Where the evolutionary link became apparent was that in cancer cell lines, unlike in tissues and primary cells, recent paralogs lacked the peak of highly correlated pairs. This novel finding suggests that global devolution and loss-of-evolutionary constraints on expression patterns accompany malignant transformation, and provides additional evidence in the debate on use of cancer cell lines as research models. &lt;br /&gt;
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&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;&amp;lt;br&amp;gt; OS and LH designed the study, performed all analyses, and wrote the manuscript. &amp;lt;br&amp;gt; A.R.R.F. and C.O.D were involved in the FANTOM5 concepts and management. &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE, TreeFam8&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Biology&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: November 30th&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Lukasz.Huminiecki@ki.se Lukasz Huminiecki] ,[mailto:oxana.sachenkova@scilifelab.se Oxana Sachenkova] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors&amp;amp;nbsp;: &#039;&#039;&#039;[[Image:The structure of animal expression pattern evolution.doc]] (only text)&amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:The structure of animal expression pattern evolution.pdf]] (this file includes all the figures) &lt;br /&gt;
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== Title:Automated clustering and quality control pipeline for CAGE technologies  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_030 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO BMC GENOMICS&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; To understand the manner and mechanisms of transcription initiation by RNA Polymerase II, different strategies for genome-wide detection of transcription start sites (TSSs) have been developed. We propose the clustering and quality control pipeline suitable for the Cap Analysis of Gene Expression (CAGE) sequence tags. The new framework uses parametric clustering at multiple scales and adopts the irreproducible discovery rate (IDR) to measure reproducibility between replicates of each cluster. Our pipeline reveals that genes have complicated structures of transcription initiation events and discover novel alternative promoters which were not detected by previous approaches. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039; Hiroko Ohmiya1, Morana Vitezic1, Martin Frith, Yoshihide Hayashizaki1, Timo Lassmann1 and many more &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:lassmann@gsc.riken.jp Timo Lassmann] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Manuscript Ohmiya Mar04.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Manuscript Ohmiya Mar04.pdf]] [[Image:Additional file2.txt]] &lt;br /&gt;
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== Title: Mesenchymal stem/stromal cells from high-grade serous ovarian cancer retain specific identity related to mesothelium  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_036 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO STEM CELLS&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;The role of cancer microenvironment is being recognized as one of the critical hallmarks in both cancer progression and metastasis. Mesenchymal Stem/Stromal Cells (MSCs) are the precursors of various cell types that compose both normal and cancer tissue microenvironments. We have isolated MSCs from various High-Grade Serous Ovarian Carcinomas (HG-SOCs), demonstrated their normal genotype, and analyzed their transcriptome with respect to similarly derived normal tissues MSCs (N-MSCs), all embedded in the large comprehensive FANTOM5 sample dataset. An integrative analysis was conducted against the extensive panel of primary cells and tissues of the FANTOM5 project that allowed us to identify a cell-type specific transcriptional activity associated with the HG-SOC-MSCs. In fact the analysis shows that HG-SOC-MSCs retain a specific identity when compared to N-MSCs and are related to the primary mesothelial or mesothelial-derived cells representing the ovarian cellular precursors. Our results support the hypothesis that HG-SOC-MSCs are bona-fide representatives of the ovarian district thus tracing their origin either to the local mesothelium or highlighting the epigenetic conditioning of externally recruited MSCs by the HG-SOC cancer cell compartment. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Roberto Verardo, Silvano Piazza, Enio Klaric, Yari Ciani, Stefania Marzinotto, Laura Mariuzzi, Daniela Cesselli, Antonio P. Beltrami, Masayoshi Itoh, Hideya Kawaji, Timo Lassmann, Piero Carninci, Yoshihide Hayashizaki, Alistair R.R. Forrest, Carlo A. Beltrami, Claudio Schneider and the FANTOM consortium &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;R.V., S.P. and C.S. designed research and analyzed all the data; R.V. followed all sample RNA/DNA quality controls; S.P. designed software, carried out statistical tests and bioinformatics analysis; Y.C. implemented part of the software and prepared some figures; E.K. performed molecular biology assays; R.V., S.M., L.M., D.C., and A.P.B. performed cell isolation and characterization, R.V., D.C., A.P.B., C.A.B. and C.S. analyzed cell-biology data; M.I. was responsible for CAGE data production; T.L. was responsible for tag mapping; H.K. managed the data handling; P.C., Y.H. and A.R.R.F. were responsible for FANTOM5 management and concept; CS supervised the whole study; R.V., S.P. and C.S. wrote the manuscript. &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on all of F5freeze1 &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;October 15th 2012 &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:schneide@lncib.it Claudio Schneider] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Claudio.pdf]] &lt;br /&gt;
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== Title: A transient disruption of a fibroblast-specific transcriptional regulatory network potently promotes trans-differentiation  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_40&amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO GENOME BIOLOGY &#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; Background: Transcriptional Regulatory Networks (TRN) coordinates multiple transcription factors (TF) in concert to maintain homeostasis and cellular function. The re-establishment of TRNs have been previously implicated in direct trans-differentiation studies where the newly introduced TFs switch-on a set of key regulatory factors to induce de novo expression and function. However, the extent to which TRNs in starting cell types, such as dermal fibroblasts, protect the cells from undergoing cellular reprogramming remains largely unexplored. Results: In order to identify specific TFs in fibroblasts, we first modeled the TRN of fibroblast cells using a Matrix-RNAi approach where 18 fibroblast-specific TFs were systematically knock-downed and profiled. The resulting expression matrix revealed 7 highly interconnected TFs as targetable factors. Interestingly, suppressing 4 out of 7 TFs generated lipid droplets and induced PPARG and CEBPA expression in the presence of adipocyte-inducing medium, while the control knockdown maintained fibroblastic characteristics in the same induction regime. The global gene expression analysis further revealed that the knockdown induced adipocytes (KDiADP) highly expressed genes associated with lipid metabolism and significantly suppressed fibroblast-specific genes. Conclusion: Overall, this study reveals the critical role of the TRN in protecting cells against aberrant reprogramming, and demonstrates, for the first time, the vulnerability of TRN, which may be a novel target to induce transgene-free trans-differentiations.  &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: Yasuhiro Tomaru, Ryota Hasegawa, Jay W. Shin , Takahiro Suzuki, Taiji Sato, Atsutaka Kubosaki, Masanori Suzuki, Yoshihide Hayashizaki and Harukazu Suzuki&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;YT designed and carried out experiments, analyzed and wrote the paper. RH carried out experiments, supported statistical analysis and wrote the paper. JS generated expression data, analyzed and wrote the paper. TS, TS and AK carried out validation of KDiADP cells. MS carried out editing of the manuscript. YH and HS coordinated all efforts and supervised the project&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Biology&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: May 20th, 2013&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:harukazu@gsc.riken.jp]Harukazu Suzuki, [mailto:jay.shin@gsc.riken.jp]Jay Shin&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:manuscript-YT-May17.docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Tomaru_F5_wiki.pdf]] &lt;br /&gt;
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== Title: Explaining the correlated properties of mammalian promoters  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_003 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Advanced draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;Proximal promoters are fundamental genomic elements for gene expression. They vary in terms of: GC percentage, CpG abundance, presence of TATA signal, evolutionary conservation, chromosomal spread of transcription start sites, and breadth of expression across cell types. These properties are correlated, and it has been suggested that there are two classes of promoter: one class with high CpG, widely spread transcription start sites, and broad expression, and another with TATA signals, narrow spread and restricted expression. It has been unclear, however, why these properties are correlated in this way. &lt;br /&gt;
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We re-examined these features using the deep FANTOM5 CAGE data from hundreds of cell types. Firstly, we point out subtle but important biases in previous definitions of promoters and of expression breadth. Secondly, we show that most promoters are rather non-specifically expressed across many cell types. Thirdly, promoters&#039; expression breadth is independent of maximum expression level, and therefore correlates with average expression level. Fourthly, the data show a more complex picture than two classes, with a network of direct and indirect correlations among promoter properties. By distinguishing the direct from the indirect correlations, we reveal simple explanations for them. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;M.C. Frith, ...? &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;All human and mouse Phase1 CTSSs &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Research(?) &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;Feb 2013 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:martin@cbrc.jp Martin Frith] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Mcf-prom-sat.pdf]] &amp;lt;br&amp;gt;&#039;&#039;&#039;Supplement: &#039;&#039;&#039;[[Image:Mcf-prom-sat-sup.pdf]] &lt;br /&gt;
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== Title: Homotypic clusters of transcription factor binding sites in the vicinity of transcription start sites  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_006 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Finished draft&amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;Background&#039;&#039; &amp;lt;br&amp;gt;Transcription factors (TFs) specifically recognizing DNA binding sites (TFBS) play a key role in regulation of gene expression. Groups of closely localized TFBSs for a particular TF, so-called homotypic TFBS clusters (HCBSs), were originally detected in yeast and extensively studied in fruit fly early development. Recently HCs were found to be highly important for several human regulatory systems. &lt;br /&gt;
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&#039;&#039;Motivation&#039;&#039; &amp;lt;br&amp;gt;It is a general practice to estimate an enrichment of binding sites in regulatory sequences. Still there is no systematized data whether the presence of HCBSs is common for promoter regions of human genes. The general properties of HCBSs also remain unclear as well as possible relation between HCBSs and regulation of tissue-specific expression. &lt;br /&gt;
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&#039;&#039;Results&#039;&#039; &amp;lt;br&amp;gt;Using data on sample-specific transcription start sites (TSSs) detected in FANTOM5 and high quality binding models for more than 400 TFs from the HOCOMOCO TFBS model collection we have predicted TFBSs and corresponding HCBSs in promoter regions surrounding TSSs. TFBS models for most TFs were shown to form statistically significant HCBSs often formed by separate distant binding sites. For HCBSs of most of TFs we were able to identify samples having significant association between promoters of sample-specific or housekeeping TSSs. Thus for most of TFs we predict putative preferences for sample-specific or housekeeping HCBSs activity and provide a genome-wide map of HCBSs nearby FANTOM5-defined TSSs. &lt;br /&gt;
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&#039;&#039;Supplementary information&#039;&#039; &amp;lt;br&amp;gt;https://fantom5-collaboration.gsc.riken.jp/webdav/home/vigg/homotypicus/ &lt;br /&gt;
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&#039;&#039;&#039;Authors: &#039;&#039;&#039;I.V. Kulakovskiy, Y.A. Medvedeva, M.S. Polishchuk, A.V. Favorov, S. Schmeier, T. Lassman, I.E. Vorontsov, RIKEN_OSC_members, V.J. Makeev &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039; IVK implemented the software and drafted the manuscript. YAM carried out statistical tests and results interpretation. MSP developed the homotypic cluster detection algorithm. AVF selected proper statistical tests. SS provided the housekeeping set of TSS-clusters. TL provided the set of sample-specific TSS-clusters. IEV estimated proper thresholds for PWMs used in the study. VJM coordinated the study. All the authors participated in writing and finalizing the manuscript. &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE - FANTOM5 FREEZE1, &amp;quot;robust&amp;quot; subset &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Nucleic Acids Research, Bioinformatics &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;18 June 2012 / Updated: 12 September 2012 / Minor fixes: 1 December 2012&amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:vsevolod.makeev@gmail.com,ivan.kulakovskiy@gmail.com Vsevolod Makeev, Ivan Kulakovskiy] &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:HOMOTYPICUS-FANTOMsatellitepaper.r1.doc]] &amp;lt;br&amp;gt; &#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:HOMOTYPICUS-FANTOMsatellitepaper.r1.pdf]] &lt;br /&gt;
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== Title: Transcriptional profiling by deep CAGE of the human fibrillin/LTBP gene family, key regulators of mesenchymal cell functions.  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID&#039;&#039;&#039;: Phase1_014 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Good Draft &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; The fibrillins and latent transforming growth factor binding proteins (LTBPs) form a superfamily of extracellular matrix (ECM) proteins characterized by the presence of a unique domain, the 8-cysteine transforming growth factor beta (TGFβ) binding domain (TB domain). These proteins are involved in both maintaining the extracellular matrix and controlling the bioavailability of TGFβ family members. Genes encoding these proteins show differential expression in mesenchymal cell types which synthesise the extracellular matrix and form connective tissues. We have investigated the promoter regions of the seven gene family members using the FANTOM5 CAGE data base for human. Although the protein and nucleotide sequences show considerable homology, the promoter regions were quite diverse. The three fibrillin genes had a single predominant promoter cluster, while LTBP1 and LTBP4 showed promoter switching. Most of the family members were expressed in a range of mesenchymal and other cell types, often associated with use of alternative promoters or transcription start sites within a promoter. FBN3 was the lowest expressed gene, and was expressed only in embryonic and fetal tissues, primarily neurological. There was evidence of enhancer activity likely to be involved in expression of the genes. Each gene showed a unique pattern of transcription factor motifs or activity. This study highlights the role of alternative transcription start sites in regulating the tissue specificity of closely related genes and suggests that this important class of extracellular matrix genes is subject to subtle regulatory variations that explain the differential roles of members of this gene family.&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors:&#039;&#039;&#039; Margaret R Davis, RIKEN OSC members, Kim M Summers&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement:&#039;&#039;&#039; MRD performed the analysis and contributed to writing the paper, RIKEN OSC did ..., KMS performed the analysis and contributed to writing the paper&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used:&#039;&#039;&#039; Helicos CAGE on ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s):&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &amp;lt;br&amp;gt;Contact by email: &#039;&#039;&#039;[mailto:kim.summers@roslin.ed.ac.uk kim.summers@roslin.ed.ac.uk]&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors:&#039;&#039;&#039; [[File:Fantom5_FBN_paper_22-08-13.doc]], [[File:Supplementary_Table_1.pdf]], [[File:Supplementary_Table_2.xlsx]], [[File:Supplementary_Table_3.xlsx]], [[File:Supplementary_Table_4.xls]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF):&#039;&#039;&#039; [[Image:Fibrillin-LTBP satellite.pdf]]&amp;lt;br&amp;gt;&#039;&#039;&#039;Revised version of paper:&#039;&#039;&#039; &lt;br /&gt;
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[[Image:Summers Phase1 014 revision 18Apr2013.pdf]] &lt;br /&gt;
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== Title: Analysis of antisense transcription in loci associated to neurodegenerative diseases  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_022 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;The FANTOM5 sequencing datasets represent the largest collection of transcriptomes from human cell lines, primary cells and whole tissues of various origin. Transcription starting sites are mapped at high resolution by the use of a modified protocol of Cap-Analysis of Gene Expression (CAGE) for high-throughput single molecule next-generation sequencing with Helicos (hCAGE). We employed the FANTOM5 collection of data to address the role of antisense transcription in neurodegeneration. We focused our analysis exclusively on tissues and primary cells, to avoid artifacts due to cellular transformation in culture cell lines. Among the &amp;amp;gt;1261 human hCAGE libraries, we selected those of brain origin. Libraries from total blood and selected blood cell populations were also included in the analysis. A total of 66 tissue- and 244 cell-specific libraries were interrogated for the presence of antisense transcription to well-established loci associated to Alzheimer’s disease, Amyotrophic Lateral Sclerosis, Frontotemporal Dementia, Huntington’s and Parkinson’s disease. Almost all analyzed genes display some degree of antisense transcription mainly in their 5’ or 3’ UTRs. 5’ head-to-head divergent antisense transcription appears enriched compared to global distribution of sense/antisense pairs. Identified antisense transcripts may have coding and non-coding capabilities, with lncRNAs being more represented. Expressed transcripts are generally poorly annotated and may contain repetitive elements of the Alu, SINE and LINE families. Antisense transcription was validated for a subset of genes, including amyloid precursor protein, microtubule-associated protein tau, DJ-1, leucin-rich repeat kinase 2 and α-synuclein. The validated transcripts are predicted to have non-coding functions and most of them were not annotated. Quantitative analysis of antisense transcripts in human tissues indicates enrichment in the brain, compatible with FANTOM 5 data. Overall, these results represent the most comprehensive analysis of antisense transcription at loci associated to neurodegeneration and provide evidence for the existence of additional regulation of disease-related genes by previously not-annotated long non-coding RNAs. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Zucchelli SIlvia, Paolo Vatta, Stefania Fedele, Raffaella Calligaris, XXXX (from F5 consortium), Al Forrest, Piero Carninci and Stefano Gustincich &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;SZ designed the experiments, analyzed the data, wrote the manuscript; PV performed the bioinformatics analysis, prepared some figures; SF designed the experiments, performed the experiments and analyzed the data; RC provided reagents, designed the experiments and analyzed the experiments; SG analyzed the data, wrote the manuscript &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on human brain and blood samples&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Research, Plos Genetics, Human Molecular Genetics&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: beginning of june&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:gustinci@sissa.it,silvia.zucchelli@sissa.it Stefano Gustincich, Silvia Zucchelli] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Zucchelli FANTOM5 Manuscript 2013 01 22.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;&amp;lt;br&amp;gt;[[Image:Zucchelli FANTOM5 Figures 2013 01 22.pdf]]&amp;lt;br&amp;gt; [[Image:Zucchelli FANTOM5 Supplementary 2013 01 22.pdf]]&amp;lt;br&amp;gt;[[Image:Zucchelli FANTOM5 TAbles 2013 01 22.pdf]] &lt;br /&gt;
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== Title:Gateways to the promoter level mammalian expression atlas covering thousands of biological states in FANTOM5  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_025 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;working draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&amp;amp;nbsp;&#039;&#039;&#039;Monitoring RNA transcribed within a cell is an essential step toward the identification of active information within the genome, and the understanding the entire cellular system ultimately. Most previous studies involving the collection of a large set of genome-wide transcription profiles consist of tissues and/or cell lines. In the FANTOM5 (Functional ANnotation Of Mammals 5) project we monitored transcription in more than one thousand mammalian samples, including nearly two hundred primary cell types in human and more than one hundred cell types in mouse. We used a sequencing-based digital counting technology, CAGE (Cap Analysis Gene Expression), which skips any PCR amplification steps relying on a single molecule sequencer. &amp;amp;nbsp;This technology quantifies transcription starting site (TSS) activities at a single base pair resolution across the genomes, and the result is one of the largest sets of expression data available, consisting of diverse range of samples with a single platform based on the state-of-the-art technology. &lt;br /&gt;
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We assembled the FANTOM5 TSS profiles and subsequent analyses into a centralized data archive and set up various on-line resources available for the scientific community. Researchers in cell biology can easily search samples of interest to inspect active elements within a cell type. Researchers in molecular biology can search genes or transcription factors of interest to inspect in which biological context they are highly activated. Researchers in genome biology and other fields can explore the data within dynamic and interactive graphical user interfaces dedicated for genomic viewing and expression. We based all analysis and database systems on careful annotation of the diverse range of samples, including an application ontology consisting of cell types, anatomy, and diseases. This large set of expression data combined with the extensive and systematic sample annotation enables the scientific community to explore, examine, and slice the data from multiple aspects. Here we introduce the on-line resources and underlying data structure as well as discuss its potential impact in multiple research fields.&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;WP4, database providers, and analysis providers&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on phase1 freeze&amp;amp;nbsp;&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;package of word, pdf, etc: &#039;&#039;&#039;[[Image:130225-F5web-resource.zip]] &lt;br /&gt;
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== Title:Application of Semantic MediaWiki to snapshot of thousands of biological states in transcription  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_026 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Unknown&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;overview and instruction to the resource browser&#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: Shimoji H, Kawaji H., WP4 &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on phase1 freeze &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title:Identification of miRNA promoters and primary structures  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_028 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Unknown&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: ...&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: Kawaji H.&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Mogrify: Defining Factors For Direct Reprogramming Between All Cell Types  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_31 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft -&amp;amp;gt; PHASE2?&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &lt;br /&gt;
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We now know that cellular state is a plastic phenomenon which it is possible to control. There are an increasing number of reports in the literature of induced pluripotency and also induced trans-differentiated from one cell type to another. Each of these experiments has relied heavily on a process of trial and error as well as expert knowledge in order to discover the transcription factors capable of inducing a cell conversion. Here we present a novel network based method (Mogrify) that can identify the factors required for cell conversion. The method compares differences in expression, as measured by FANTOM5 CAGE data, over interaction networks. It provides candidate combinations of transcription factors for over-expression and knock-down, along with the likelihood score for conversion between any two given cell types. &lt;br /&gt;
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We show that the method reproduces known reprogramming factors for several successful trans-differentiations from the literature (eg between fibroblast and cardiomyocyte, neuron and hepatocyte); we discuss alternative combinations that Mogrify suggests for these conversions and for other conversions which have some experimental data in the literature but for which a fully successful differentiation is yet to be published. &lt;br /&gt;
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The technique is then run without human intervention on every possible pairwise combination of over 1000 libraries in the FANTOM 5 set, assessing possible combinations of factors for perturbation, and associating a likelihood score for success. This information is then used to construct a computational “Waddington landscape”, identifying the best candidate source and target cell types for future cell conversion experiments. This is the first resource of it’s kind, only made possible by the new FANTOM5 promoterome data and represents a considerable step forward in computational cell reprogramming. &lt;br /&gt;
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.&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Owen and Julian &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks in all samples &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:owen.rackham@bristol.ac.uk,gough@cs.bris.ac.uk Owen Julian] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Mogrify.pdf]] &lt;br /&gt;
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== Title: Investigating tissue-specificity of cancer-causing mutations  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_037 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Over the past 10 years an increasing number of mutated genes have been associated with familial predisposition to cancer. Interestingly for more than half of these genes their involvement in cancer is restricted to only a few cancer types (e.g. BRCA1 mutations in breast and ovarian cancers). Even more interestingly some of these genes are expressed in all cell types, and perhaps we would expect to see them causing many more different types of cancer but they don’t. This paper will examine how these mutations are tolerated in most cell types but not in others by considering the network of genes expressed in different cell types and how that determines whether they are susceptible or resistant. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Jessica Mar, Daniel Carbajo, RIKEN_OSC_members, Alistair Forrest &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;JM and AF conceived the project, DC conducted the analyses. &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:jessica.mar@einstein.yu.edu Jessica Mar] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title:FANTOM5 reveals the genomic architecture of the genes implicated in Rett Syndrome  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_038 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Manuscript&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; Mutations in MECP2, FOXG1 and CDKL5 genes cause Rett Syndrome, a neuro-developmental disorder of the grey matter of the brain that almost exclusively affects females. We analyzed the RNA expression data from the FANTOM5 project in both human and mouse to investigate the genomic architecture of the three genes involved in Rett syndrome. Data from FANTOM 5 provides the unprecedented opportunity to study the expression profile, identify transcription start sites and, in conjunction with the recently released ENCODE dataset, identify the regulatory regions and transcription regulators of the three genes implicated in Rett Syndrome. Even though MECP2 and CDKL5 are expressed ubiquitously, mutations in these genes cause a brain specific phenotype suggesting that their role in brain is distinctly important from their function in other tissues. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors:&#039;&#039;&#039; Morana Vitezic, Leonard Lipovitch, Alistair RR Forrest, Piero Carninci, Alka Saxena &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; NAR &amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; December 2012 &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:mvitezic@gmail.com,alka@gsc.riken.jp Morana Vitezic Alka Saxena] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Rett paper.doc]] [[Image:Rett paper figures.zip]] [[Image:Rett paper supplementary.zip]]&amp;lt;br&amp;gt;&lt;br /&gt;
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== Title: Tissue gene expression profiles in relationship to primary cell gene expression profiles  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_039&amp;lt;br&amp;gt; &#039;&#039;&#039;Status:&#039;&#039;&#039; Initiated&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; Gene expression profile in a particular tissue determines the functionalities and signature properties in contrast with other tissues within the same organism. It is uncertain whether gene expression profiles in tissues are simply the results of a combination of gene expressions of the group of constituting primary cells, or if gene expression profiles differ when primary cells have been isolated from the tissues. In this paper, we would like to investigate the gene expression profiles of primary cells in relationship to tissue expression profiles. We are interested in finding out what kind of genes are involved in the differences and what functions they might have. We aim to find out to what degree do tissues resemble the sum expression of its composing cells, and if there are genes that are expressed in a tissue environment only.&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Nancy Yu, Carsten Daub, possibly members from the Human Protein Atlas (HPA) group. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement:&#039;&#039;&#039; NY will plan, perform most of the bioinformatics analyses and write the manuscript. CD will supervise the bioinformatics analysis, contribute additional ideas, and assist with manuscript writing. The HPA group will supply some data and possibly contribute to the bioinformatics analyses. &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used:&#039;&#039;&#039; Phase1 CAGE peaks and possibly HPA RNA-Seq data&amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s):&#039;&#039;&#039; Genome Research / PLoS Genetics / Genome Biology &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date:&#039;&#039;&#039; 2014 &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email:&#039;&#039;&#039; [mailto:nancy.yu@ki.se,carsten.daub@ki.se Nancy Yu, Carsten Daub] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors:&#039;&#039;&#039; [[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt; &#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF):&#039;&#039;&#039; [[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title:Pan Cancer Biomarkers and Disruption of Gene Regulatory Networks in Cancer.  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_41 &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039;CAGE FANTOM5 data collection of cancer cell lines and corresponding primary cells enables us to study the changes in transcription and gene regulation that occur in cancer and drive its development. CAGE is a 5’ sequence tag technology and provides us with a snapshot of genome-wide transcription start sites and shows in unbiased way which parts of genome are being actively transcribed into RNA in any given biological state. We analysed the CAGE data from 123 cell lines representing 12 different cancer types and compared them to the corresponding normal/primary cells (141 samples). We show the protein coding genes and non-coding RNAs that are up-regulated or down-regulated across multiple cancer types and therefore are candidates for pan cancer biomarkers. Furthermore, we show the changes in transcription factor activities and enhancer usage in cancers as well as disruption in gene co-regulation. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039;  Bogumil Kaczkowski, the FANTOM5 consortium and Alistair Forrest&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;  &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:forrest@gsc.riken.jp] &lt;br /&gt;
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== Title: Pathogen specific monocyte transcriptional responses  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_008 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Wells &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:c.wells@uq.edu.au,a.beckhouse@uq.edu.au Christine Wells, Anthony Beckhouse] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Promoter specificity in transcription determines cell lineage choice  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_018 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Delayed (as of September 12th)&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;This paper will use pathprint (pathway fingerprinting) to develop an overall phylogenetic tree of all samples in F5 freeze1. This tree will be used to determine relative ancestry of samples and cluster them accordingly. SwitchEngine will be run to find switching in TSS at key junctions in differentiation. Will show TSS dynamics at these informative sites is associated with lineage-commitment. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Emmanuel Dimont, Gabriel Altschuler, Winston Hide&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;ED did ..., GA did ..., WH did ...&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on all of F5freeze1 &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:edimont@hsph.harvard.edu,gabrielaltschuler@googlemail.com,whide@hsph.harvard.edu Winston Hide, Emmanuel Dimont, Gabriel Altschuler]&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Gene duplication and promoter divergence in mammals.  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_020&amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Delayed&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Lukasz Huminiecki and Core RIKEN Authors &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... and LH did everything else&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ..., F5 promoter and enhancer datasets, TreeFam8&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Research&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: September 1st&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Lukasz.Huminiecki@ki.se Lukasz Huminiecki] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Gene duplication and TF/miRNA regulatory network evolution in mammals.  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_021 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Delayed&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Lukasz Huminiecki and Core RIKEN Authors &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... and LH did everything else&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ... TreeFam8, miRBase, microRNA target predictions&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Research&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: December 1st&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Lukasz.Huminiecki@ki.se Lukasz Huminiecki] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Higher order chromatin structure and promoter activity  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_023 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Delayed -&amp;amp;gt; moved to PHASE2 &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Semple CA, Prendergast JG, et al &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: October 2012&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Colin.Semple@igmm.ed.ac.uk,prenderj@gmail.com Colin Semple, James Prendergast] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
&lt;br /&gt;
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&lt;br /&gt;
== Title:Building context depending TSS regions from thousands of profiles  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_024 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Unknown&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;about DPI &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Kawaji H, et al. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on phase1 freeze &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
&lt;br /&gt;
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&lt;br /&gt;
== Title: Quantifying the informational complexity of transcriptional regulatory programmes  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_015 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;On-hold. Focussing on the biological results Phase1_016 rather than methods. Hope to return to methods later (phase2).&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; The regulation of gene expression defines cellular identity, it is the basis for organism development and it underlies many cellular responses to the environment. Its disruption is implicated in many diseases and changes in gene regulation appear to underlie many adaptations evident between species. Previously, genes have been grouped and interpreted based on their specificity of expression, for example house-keeping genes that are expressed by all cells in all conditions versus highly tissue restricted genes expressed by only one cell type at a particular developmental time. Although such studies have been informative they fail to capture important aspects of how a gene is regulated or account for the heterogeneous relatedness of samples. The expression pattern of a gene is the output of a regulatory program within the cell. A program that must affect many state changes (on, off, up, down) is likely to require more regulatory information (Kolmogorov complexity) than a program effecting fewer state switches. If we can quantify this &amp;quot;regulatory complexity&amp;quot; we can then start to address deeper questions as to where that regulatory information is encoded, how malleable it is through evolution and how susceptible it is to perturbation by mutation. For example, a greater regulatory complexity could correspond to a higher concentration of cis-regulatory sequences around the gene or alternatively a single binding site for a transcription factor that is the output of an extensive intracellular signalling network. To address these questions we have explored a range of possible measures regulatory complexity including distance weighted entropies, diversity and richness scores. This leads us to introduce a novel measure of regulatory complexity (CR). It is implemented as a hierarchical Baysian model parametrised through MCMC. The CR method can be thought of as a relative measure of the number of gene expression state changes occurring over a tree relating all analysed samples. A by-product of this analysis is a probabilistic scoring of gene expression state switches between all analysed gene expression libaries. CR is weighted to account for the genome wide similarity of gene expression between samples but does not depend on the inference of a fixed underlying tree topology. &amp;lt;font color=&amp;quot;green&amp;quot;&amp;gt;Note - this is intended as essentially a methods paper, see Phase1_016 for the biological insights paper&amp;lt;/font&amp;gt; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Sarah Baker, Martin Taylor &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;SB developed and implemented methods and performed general analyses; MT conceived the project and oversaw implementation and performed some of the analysis&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on primary cells from human and mouse.&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Bioinformatics or Genome Research&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date:&#039;&#039;&#039; ETA July 2013 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:martin.tayor@igmm.ed.ac.uk,sarah.baker@igmm.ed.ac.uk Martin Taylor, Sarah Baker]&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
&lt;br /&gt;
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&lt;br /&gt;
== Title: Cis encoding of the master developmental regulatory programme  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_016 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft, starting dataset being regenerated to incorporate improved method&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; The regulation of gene expression defines cellular identity, it is the basis for organism development and it underlies many cellular responses to the environment. Its disruption is implicated in many diseases and changes in gene regulation appear to underlie many adaptations evident between species. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Sarah Baker, Martin Taylor &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;SB developed and implemented methods and performed general analyses; MT conceived the project and oversaw implementation and performed some of the analysis&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on primary cells from human and mouse. We may also want to use time course data for this paper (does that push it into phase2?).&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;PLoS Biology&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date:&#039;&#039;&#039; ETA March 2013 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:martin.tayor@igmm.ed.ac.uk,sarah.baker@igmm.ed.ac.uk Martin Taylor, Sarah Baker]&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
&lt;br /&gt;
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&lt;br /&gt;
&lt;br /&gt;
== Title: Comparison of CAGE and RNA-Seq profiling results for human tissue and cell line data ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_042 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status:&#039;&#039;&#039; Initiated&amp;lt;br&amp;gt;&#039;&#039;&#039;Abstract:&#039;&#039;&#039; A systematic comparison of CAGE and HPA RNA-Seq tissue and perhaps cell line dataset, since both datasets will probably serve as widely used gene expression resources for the research community. This study will inform the researchers of the features of each dataset, including consensus and individual strengths of each data source. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039; Nancy Yu, Carsten Daub, possibly members from the Human Protein Atlas (HPA) group. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;NY will plan, perform most of the bioinformatics analyses and write the manuscript. CD will supervise the bioinformatics analysis, contribute additional ideas, and assist with manuscript writing. The HPA group will supply some data and possibly contribute to the bioinformatics analyses. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039; phase1 CAGE peaks, HPA RNA-Seq data &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; early 2014 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:nancy.yu@ki.se,carsten.daub@ki.se Nancy Yu, Carsten Daub] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
&lt;br /&gt;
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&lt;br /&gt;
== Title:CAGExploreR: an R package for the analysis and visualization of promoter dynamics across multiple experiments  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID&#039;&#039;&#039;&#039;&#039;: &#039;&#039;Phase1_043 &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;NOTE:&#039;&#039;&amp;amp;nbsp;This is a paper describing what used to be called &amp;quot;SwitchEngine&amp;quot;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;&#039;&#039;Status: &#039;&#039;&#039;Complete. Ready for Submission. &amp;lt;br&amp;gt;&#039;&#039;&#039;Abstract: &#039;&#039;&#039;Alternate promoter usage is an important molecular mechanism for generating RNA and protein diversity. Cap Analysis Gene Expression (CAGE) is a powerful approach for revealing the multiplicity of transcription start site (TSS) events across experiments and conditions. An understanding of the dynamics of TSS choice across these conditions requires both sensitive quantification and comparative visualization. We have developed CAGExploreR, an R package to detect and visualize changes in the utilization of specific TSS in wider promoter regions in the context of changes in overall gene expression when comparing different CAGE samples. These changes provide insight into the modification of transcript isoform gen-eration and associated regulatory network alterations associated with cell types and conditions. CAGExploreR is based on the FANTOM5 and MPromDb promoter set definitions but can also work with user-supplied regions. The package compares multiple CAGE libraries simultaneously and does not require replicates. Online supplementary materials describe methods in detail and a vignette demonstrates a workflow with a real data example.&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Emmanuel Dimont, Alistair R. R. Forrest, Hideya Kawaji, Winston Hide and the&amp;amp;nbsp;FANTOM Consortium&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;ED developed the method, the R package (software), wrote the paper and supplementary materials plus figures, AF created the original idea and provided data, HK created DPI TSS&amp;amp;nbsp;clusters (promoters), WH formulated the idea, wrote the paper and provided funding, FC provided funding and data.&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 DPI clusters, ENCODE CAGE data for MCF7 and A549 cell lines&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Bioinformatics&amp;amp;nbsp;(Application Note)&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;October 7th, 2013&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;Emmanuel Dimont (edimont@mail.harvard.edu)&amp;amp;nbsp;&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;The latest version of the manuscript, supplementary methods, R&amp;amp;nbsp;package and vignette can be found at [https://www.dropbox.com/sh/h9bf81ia56ywskq/gMPZ2KVfmi here].&amp;amp;nbsp;&amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;see above&#039;&#039;&#039;&amp;amp;nbsp;&#039;&#039;&#039; &lt;br /&gt;
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&lt;br /&gt;
== Title:COPY THEN EDIT THIS TEMPLATE  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_00x (INCREMENT THIS) &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: ...&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: R&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:blah@change.this.edu,next.adress@change.this CHANGETHIScorresponding1 CHANGETHIScorresponding2] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_submission&amp;diff=7053</id>
		<title>Satellite submission</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_submission&amp;diff=7053"/>
		<updated>2013-11-05T12:37:01Z</updated>

		<summary type="html">&lt;p&gt;Yulia: /* Title: Effect of cytosine methylation on transcription factor binding sites and regulation of transcription */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;== Satellite manuscript internal review page  ==&lt;br /&gt;
&lt;br /&gt;
Welcome to the FANTOM5 Satellite review page. As discussed at the Ume and Koyo meetings, all papers will be visible to consortium members. This is to allow everyone to know what is going on, promote collaboration, carry out due process regarding co-authorship and to avoid competition. &lt;br /&gt;
&lt;br /&gt;
== Authorship  ==&lt;br /&gt;
&lt;br /&gt;
The author list will basically be selected by the first author and the corresponding author of each satellite paper on the basis of the scientific contribution to the manuscript. Remember to include an authors contribution statement for all authors named in your manuscript (of the form AB carried out the cell isolation, SB carried out the network predictions etc.). &lt;br /&gt;
&lt;br /&gt;
In addition the FANTOM5 headquarter will name RIKEN OSC members who should be co-authors for their input on each manuscript and to the entire FANTOM5 project. For those of you who have participated in previous FANTOMs you will be familiar with this process, for those new to FANTOM please look at the author lists on the satellite paper collections for FANTOM2-4. FANTOM5 headquarter is currently discussing the policy for RIKEN OSC co-authorship on the FANTOM5 satellites, but basically satellites papers will be considered on a case by case basis, and will take into account datasets used, intellectual input and facilitating technologies/analyses for each paper. &lt;br /&gt;
&lt;br /&gt;
At this stage please name any authors from the OSC that you think should definitely be included as co-authors, in addition for all satellite submissions include the following term &#039;&#039;&#039;RIKEN_OSC_members&#039;&#039;&#039; as an additional author. &lt;br /&gt;
&lt;br /&gt;
== Instructions  ==&lt;br /&gt;
&lt;br /&gt;
Please make a copy of the template below and enter your manuscript details. &lt;br /&gt;
&lt;br /&gt;
If you are not able to edit the wiki yourself please email the secretariat with the subject line &amp;quot;FANTOM5_satellite&amp;quot;, but please understand that these will be processed when we can rather than immediately. You must fill in all of the details below and provide both a PDF that contains all figures, and word doc of the main text, for reviewers to mark up directly. &lt;br /&gt;
&lt;br /&gt;
== RIKEN affiliation and acknowledgements in Satellite papers - guidelines ==&lt;br /&gt;
&lt;br /&gt;
As of April 1st, 2013, Omics Science Center has ceased to exist as a part of RIKEN reorganization. Many OSC members have changed their affiliation to other RIKEN centers or institutions. Therefore there has been a change in the way affiliations and acknowledgements are written on the Phase 1 satellite papers.&lt;br /&gt;
&lt;br /&gt;
Please consult the below guidelines before submitting the paper. For the existing manuscripts/manuscripts under submission please change affiliations and acknowledgements accordingly.&lt;br /&gt;
&lt;br /&gt;
Also, authors should &#039;&#039;&#039;send the manuscripts to &#039;&#039;&#039;[mailto:fantom5-secretariat@gsc.riken.jp FANTOM5 Secretariat] for checks before submitting the paper or the final proof to avoid trouble later.&lt;br /&gt;
&lt;br /&gt;
Guidelines: [[File: F5_affiliation_acknowledgements_130816.pdf]]&lt;br /&gt;
&lt;br /&gt;
= Manuscripts  =&lt;br /&gt;
&lt;br /&gt;
== Title: Epigenetic factors regulating Hematopoiesis  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_004 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;The hematopoietic differentiation pathway is a complex regulatory program for generating different lineages of blood cell types from multipotent, hematopoietic stem cells. The transcriptional program dictating hematopoietic cell fate and differentiation requires an epigenetic memory function consisting of a network of enzymes controlling DNA methylation, histone posttranslational modifications and chromatin structure. Defective interactions between epigenetic enzymes and transcription factors cause perturbations in blood cell differentiation, which often leads to various types of hematopoietic disorders such as leukemia. To elucidate the contribution of different epigenetic factors in human hematopoieis, high-throughput Cap Analysis of Gene Expression (CAGE) sequencing was used to build comprehensive transcription profiles of 199 epigenetic factors in a wide range of blood cells. These epigenetic factors include proteins that covalently modify DNA/histones or alter chromatin structure dynamics. Our analysis revealed several epigenetic factors to have expression profiles specific for cell type, lineage type and/or leukemic cell lines. In this report the ‘epigenetic transcriptome’ has been systematically studied to predict their potential functions in the epigenetic regulatory network of human hematopoiesis. The potential of such a comprehensive study is not only to identify putative epigenetic regulators of normal hematopoiesis and postulate their function but also to serve as a resource for the scientific community for further characterization and validation of differentially expressed transcripts. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Punit Prasad, Michelle Rönnerblad,...FANTOM5, Erik Arner, Karl Ekwall and Andreas Lennartsson &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;PP and MR have done analysis and written the manuscript. EA has performed the initial CAGE analysis for the epigenetic factors and assisted in writing the manuscript. AL and KE have assisted in writing the manuscript, planned and coordinated the study. The authors declare no conflict of interest.&amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ... &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Blood or other&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;December 06, 2012&amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:andreas.lennartsson@ki.se,arner@gsc.riken.jp Andreas Lennartsson, Erik Arner] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Prasad et al Blood 020213 .docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Prasad et al Blood 020213 .pdf]] &lt;br /&gt;
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== Title: Redefinition of the human mast cell transcriptome by deep-CAGE sequencing ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_009 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;Despite their haematopoietic origin, mast cells (MCs) mature exclusively in peripheral tissues, hampering research into their developmental and functional programs. Here, we employed deep-CAGE on skin-derived MCs to generate the most comprehensive view of the human MC transcriptome ever reported. A particular advantage is that MCs were embedded in the FANTOM5 project, giving the opportunity to contrast their molecular signature against an extensive panel of human samples. We demonstrate that MCs possess a unique and surprising transcriptional landscape, combining expression of typical haematopoietic genes with those exclusively active in MCs, and genes not previously reported as expressed in MCs. Specifically we found that MCs express functional BMP receptors, which transduce pro-survival and activatory signals. Conversely, several genes frequently studied in MCs were either not or only weakly expressed in direct comparison with other myelocytes. By the parallel use of MCs ex vivo and following culture, we also found that MCs change their transcriptome in in vitro surroundings. Befitting their uniqueness, MCs had no close relative in the haematopoietic network. This rich dataset reveals that our knowledge of human MCs is still fairly limited. It can be anticipated that with this resource novel functional programs of MCs will soon be discovered.&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Efthymios Motakis,1,* Sven Guhl,2,* Yuri Ishizu,1 RIKEN OSC members,1 Torsten Zuberbier,2 Alistair R R Forrest,1¶ Magda Babina2¶&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;E.M. carried out bioifnormatics analayses S.G. isolated the mast cells and performed most experiments, M.B. performed several experiments, was involved in planning, supervision, and data analysis, and wrote the first draft of the manuscript, E.M. S.G., A.R.R.F. and T.Z. helped with planning, data analysis and manuscript writing. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on mast cell samples in comparison to freeze 1 data &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Blood, eBlood &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:magda.babina@charite.de,sven.guhl@charite.de Magda Babina, Sven Guhl] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:BLOOD-2013-483792v1-Forrest.pdf]] &lt;br /&gt;
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== Title: Transcription and enhancer profiling in human monocyte subsets  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_011 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Human blood monocytes comprise at least three subpopulations that differ in phenotype and function. Here we present the first in-depth regulome analysis of classical (CD14++CD16-), intermediate (CD14+CD16+), and nonclassical (CD14dimCD16+) monocytes. Cap Analysis of Gene Expression (CAGE) adapted to Helicos single molecule sequencing was used to map transcription start sites throughout the genome in all three subsets. In addition, global maps of H3K4me1 and H3K27ac deposition were generated for classical and nonclassical monocytes defining enhanceosomes of the two major subsets. We identify differential regulatory elements (including promoters and putative enhancers) that were associated with subset-specific motif signatures corresponding to different transcription factor activities and exemplarily validate a novel downstream enhancer of the CD14 locus. In addition to known subset specific features, pathway analysis revealed marked differences in metabolic gene signatures. While classical monocytes expressed higher levels of genes involved in carbohydrate metabolism priming them for anaerobic energy production, nonclassical monocytes expressed higher levels of oxidative pathway components and showed a higher routine mitochondrial activity. Our findings describe promoter/enhancer landscapes and provide novel insights into the specific biology of human monocyte subsets. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Christian Schmidl, Kathrin Renner, Ruediger Eder, Katrin Peter, Petra Hoffmann, Reinhard Andreesen, Marina P. Kreutz, RIKEN_OSC_members, Matthias Edinger, Michael Rehli &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;CS performed experiments, computational analyses and wrote parts of the manuscript writing, KR performed experiments and contributed to manuscript writing, RE isolated the cells, KP performed experiments, PH, RA, MK, and ME contributed to planning and supervision, RIKEN_OSC_members who organized or performed Helicos sequencing and provided aligned data; MR initiated, planned and supervised the study, performed computational analyses, and wrote the manuscript. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on monocyte subsets (Regensburg samples) &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Blood, eBlood, other &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: September 1 ,2012 &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:michael.rehli@ukr.de,Christian.Schmidl@klinik.uni-regensburg.de Michael Rehli, Christian Schmidl] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Schmidl MonoSub.docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Schmidl MonoSub.pdf]]&amp;amp;nbsp;&amp;amp;nbsp; &lt;br /&gt;
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== Title:The enhancer and promoter landscape of regulatory and conventional T cell subpopulations  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_34&amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; CD4+CD25+FOXP3+ human regulatory T cells (Treg) are essential for self-tolerance and immune homeostasis. Here, we describe the promoterome of CD4+CD25highCD45RA+ naïve and CD4+CD25highCD45RA– memory Treg and their CD25– conventional T cell (Tconv) counterparts both before and after in vitro expansion by cap analysis of gene expression adapted to single molecule sequencing (HeliscopeCAGE). We performed comprehensive comparative digital gene expression analyses and revealed new orphan transcription start sites, of which several were validated as alternative promoters of known genes including FOXP3 and CTLA4. For all in vitro expanded subsets, we additionally generated genome-wide maps of poised and active enhancer elements marked by histone H3 lysine 4 monomethylation and histone H3 lysine 27 acetylation. Analysis of cell type-specific regulatory elements revealed a specific enrichment of several transcription factor binding motifs. We validated promising candidates by chromatin immunoprecipitation coupled to next generation sequencing and identified STAT5 and FOXP3 as well as RUNX1 and ETS1 as global regulators of Treg- and Tconv-specific enhancers, respectively. In summary we provide a highly detailed and easily accessible resource of gene expression and -regulation in Treg and Tconv subpopulations. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: R&#039;&#039;&#039; &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Blood&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:christian.schmidl@klinik.uni-regensburg.de,michael.rehli@klinik.uni-regensburg.de Christian Schmidl, Michael Rehli] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:121027 FANTOM Treg manuscript.docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Schmidl Treg.pdf]] &lt;br /&gt;
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== Title: Effect of cytosine methylation on transcription factor binding sites and regulation of transcription  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_010 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BMC GENOMICS&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Background: DNA methylation in promoters is strongly linked to downstream gene repression. However, the question remains as to whether DNA methylation is a cause or a consequence of gene repression. In the former case, DNA methylation may affect the affinity of transcription factors (TFs) towards their binding sites (TFBSs). In the latter case, gene repression caused by chromatin modification is stabilized by DNA methylation. Until now, the above-mentioned scenarios have been only supported only by non-systematic evidences and have not been tested for a wide spectrum of TFs. Although the average promoter methylation is usually used in related studies, recent results suggested that methylation of individual cytosines can be also important. &amp;lt;br&amp;gt; Results: We found that for 16.6% of cytosines methylation profile and the expression profile of neighboring TSSs were significantly anti-correlated. We named CpG corresponding to such cytosines as “traffic lights”. We observed a strong selection against CpG “traffic lights” within TFBSs. The negative selection was stronger for transcriptional repressors as compared to transcriptional activators or multifunctional TFs as well as for core TFBS positions as compared to flanking TFBS position.&amp;lt;br&amp;gt; Conclusions: Our results indicate that direct and selective methylation of certain TFBS that prevents TF binding is restricted to only special cases and cannot be considered as a general regulatory mechanism of transcription.&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Yulia A Medvedeva, Abdullah Khamis, Ivan V Kulakovskiy, Wail Ba-Alawi, Md Shariful I Bhuyan, Hideya Kawaji, Timo Lassmann, Matthias Herbers, Alistair RR Forrest, Vladimir B Bajic and the FANTOM consortium&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;YAM designed the computational experiments, selected and preprocessed the data, produced statistical analysis and wrote the manuscript; AK performed most of the data analysis; WBA and MdSIB contributed RDM models and tools for threshold estimation and mapping; [potential F5 collaborators], IVK performed part of the analysis, contributed to the design of the experiments and writing of the manuscript; VBB contributed to the design of the experiments and writing of the manuscript. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on 50 sample types, ENCODE RRBS data for the same samples &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Genome biology&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;December, 16 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:ju.medvedeva@gmail.com Yulia Medvedeva] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Effect of cytosine methylation on transcription factor binding sites and regulation of transcription.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Effect of cytosine methylation on transcription factor binding sites and regulation of transcription.pdf]] &amp;lt;br&amp;gt;&#039;&#039;&#039;Additional files for general viewing: &#039;&#039;&#039;[[Image:Effect of cytosine methylation on transcription factor binding sites Additional files.zip]] &amp;lt;br&amp;gt; &amp;quot;Accepted version:&amp;quot; [[Image:Medvedeva et al_ accepted.zip]]&lt;br /&gt;
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== Title: The Evolution of Human Cells in terms of Protein Innovation  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_013 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT MOLECULAR BIOLOGY AND EVOLUTION&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Humans are complex organisms composed of a great many cell types. Since the genomic DNA of each cell is identical, cell type is determined by what is expressed. We examine the evolutionary history of each human cell type at the molecular level via the collective histories of proteins, the principal product of gene expression. Sequence data from the FANTOM5 consortium are used to provide cell-type specific digital expression of protein-coding genes, and the SUPERFAMILY and dcGO resources provide domain and function annotation respectively. Cross-referencing with the domain annotation of all other completely-sequenced genomes provides the evolutionary context for each protein. We combine all of this to generate a description of cellular evolution at the molecular level. &lt;br /&gt;
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We present a protein domain view of the evolution of cell type. To achieve this we first identify the most recent common ancestor (MRCA) or ‘creation epoch’ of every protein in the repertoire of the human genome. We are then able to use the protein creation epochs to describe the history of the emergence of each cell type over evolution in terms of the collective histories of the proteins expressed in that cell type. Each cell type has an evolutionary profile consisting of a timeline along the lineage from the ancient cellular ancestor to modern day human. The profile of each cell type shows at which epochs along the timeline innovations in protein evolution took place; required to allow the observed expression in that type of cell. By clustering cell types on these profiles, we find groups of cell types that share a parallel protein evolutionary history and thus potentially possess a common progenitor cell type or are evolving in cooperation. A functional enrichment analysis of these clusters reveals key proteins responsible for evolutionary shifts and functional innovations; it also suggests a possible order in which different cells could have emerged during evolution, which we discuss in relation to the human immune system. The structural domain-centric perspective which we employ in this work can also be used as the basis for a comparison of the molecular basis of functional and phenotypic differences between cell types within these evolutionary clusters, exemplified by an inspection of our results on different regions of the brain. &lt;br /&gt;
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We present a view of the landscape of nature’s innovation of protein structure and architecture required to explain the creation of the different human cell types. This landscape has some important features such as the possibility that the last universal ancestor of life provided most of the innovation for the innate immune system whilst brain cells have been making use of novel proteins that first appeared in opisthokonta (animals and fungi) and continued to do so right up until homo sapiens. The landscape also lends itself to identifying candidate genes for disease by highlighting those that were important in enabling certain phenotypic shifts at key points in evolution.&amp;lt;br&amp;gt; &lt;br /&gt;
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Authors: &#039;&#039;&#039;Adam J. Sardar, Matt E. Oates, Hai Fang, Alistair R.R. Forrest,Hideya Kawaji, Julian Gough, Owen J.L. Rackham and the FANTOM Consortium&#039;&#039;&#039; &lt;br /&gt;
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Authors contribution statement: FANTOM5 was made possible by a Research Grant for RIKEN Omics Science Center from MEXT to Yoshihide Hayashizaki and a Grant of the Innovative Cell Biology by Innovative Technology (Cell Innovation Program) from the MEXT, Japan to Y.H.. We would like to thank all members of the FANTOM5 consortium for contributing to generation of samples and analysis of the dataset and thank GeNAS for data production. A.J.S. and M.E.O. were funded by BCCS studentships from EPSRC [EP/E501214]; another funding source was the BBSRC [BB/ G022771/1 to J.G., funding O.J.L.R. and H.F.].The authors would like to thank David de Lima Morais for useful discussion at the preliminary stages of this work. &amp;lt;br&amp;gt; Datasets used: &#039;&#039;&#039;Helicos CAGE on all samples &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s):&#039;&#039;&#039;GR&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:gough@compsci.bristol.ac.uk,owen.rackham@gmail.com Julian Gough, Owen Rackham] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Rough draft available on request]] &amp;lt;br&amp;gt; &#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): submitted revisions: [[Full_Manuscript_Sardar_et_al.pdf‎]] &#039;&#039;&#039;[[Image:TraP Journal Submission.zip]]&#039;&#039;&#039; [[Image:GR Submission 3 March Sardar 2013 The Evolution of Human Cells in terms of Protein Innovation.pdf]] &lt;br /&gt;
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== Title:Comparison of CAGE and RNA-seq transcriptome profiling using a clonally amplified and single molecule next generation sequencing  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_027 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT GENOME RESEARCH&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; CAGE (Cap Analysis Gene Expression) and RNA-seq are two major technologies used for transcript quantification. These protocols measure expression by from either the 5’ end of capped molecules (CAGE) or tags randomly distributed along the length of a transcript (RNA-seq). Library protocols for clonally amplified (Illumina, SOLiD, 454, Ion Torrent) 2nd generation sequencing platforms typically employ PCR pre-amplification prior to clonal amplification, while 3rd generation single molecule sequencers can sequence unamplified libraries. While these protocols individually have been demonstrated to be highly reproducible, no systematic comparison has been carried out between the protocols. Here we compare CAGE using both 2nd and 3rd generation sequencers and RNA-seq using a 2nd generation sequencer based on a panel of RNA mixtures from two human cell lines (THP-1 and HeLa, 100%, 50%, 20%, 10%, 5%, 1% and 0% of HeLa RNAs) to examine power to discriminate biological states, to detect differentially expressed genes, linearity of measurements as well as quantification reproducibility. Quantification by CAGE with the 2nd and 3rd generation sequencers (Illumina GA-IIx and HeliScope) were consistent at gene level, however we observed several differences, which can be explained by differences in their protocols and sequencing platforms. These include significant bias in the Illumina library, such as GC biases and over-estimation of transcripts harboring internal Ecop15I sites., A poorer correlation at the level of individual TSS positions, which is likely to be due to higher indel rate in HeliScope, is also found. We found high consistency between HeliScopeCAGE with RNA-seq (spearman correlations 0.88). Differences between CAGE and RNA-seq are explained by incompleteness of existing gene models in most cases, where 5’-ends of gene models do not reflect actual transcription starting site in the profiled cells, or RNA polymerase run through the poy adenylation site resulting in fusion of neighboring genes. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;WP3 &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;Genome Res. &#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: 23rd Dec, 2012 &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Submitted PDF: &#039;&#039;&#039;[[Image:130215-PlatformEval-submittedGR.pdf]]  &lt;br /&gt;
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== Title: Differential roles of epigenetic conversion and Foxp3 expression in regulatory T cell-specific transcriptional regulation  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_029 &amp;lt;br&amp;gt; &lt;br /&gt;
&#039;&#039;&#039;Status: ACCEPTED AT PNAS&#039;&#039;&#039;&amp;lt;br&amp;gt;&lt;br /&gt;
&#039;&#039;&#039;Abstract: &#039;&#039;&#039;Naturally occurring regulatory T (Treg) cells are engaged in the maintenance of immune tolerance and homeostasis. The development of Treg cells requires both the expression of the transcription factor Foxp3 and the establishment of Treg cell-type DNA hypomethylation pattern. By transcriptional start site (TSS) cluster analysis, we here assessed possible correlation of genome-wide DNA methylation pattern or Foxp3-binding pattern with Treg-specific gene expression. We found that Treg cell-specific DNA hypomethylated regions were closely correlated with Treg-upregualted TSS clusters, whereas Foxp3-binding regions had no significant correlation with either up- or down-regulated clusters, in non-activated Treg cells. On the other hand, in activated Treg cells, Foxp3-binding regions showed a strong correlation with down-regulated clusters. In silico search for transcription factor-binding motifs revealed that the motifs enriched in Foxp3-binding or Treg-specific DNA hypomethylated regions were mostly different. These results collectively indicate that Treg cell-specific DNA hypomethylation is conducive to up-regulation in the steady state Treg cells whereas Foxp3 expression to down-regulation of its target genes in activated Treg cells. Thus, the combination of the two events is required for the establishment of Treg cell-specific gene expression and function. &lt;br /&gt;
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&#039;&#039;&#039;Authors: &#039;&#039;&#039;Hiromasa Morikawa1,2, Naganari Ohkura1, Alexis Vandenbon3, RIKEN_OSC_members 4, Daron Standley3, Hiroshi Date2, Shimon Sakaguchi1 &lt;br /&gt;
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1. Department of Experimental Immunology, World Premier International Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan&amp;lt;br&amp;gt;2. Department of Thoracic Surgery, Kyoto University, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan&amp;lt;br&amp;gt;3. Department of Systems Immunology, World Premier International Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan&amp;lt;br&amp;gt;4. RIKEN Omics Center, Yokohama, Japan&amp;lt;br&amp;gt;&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &amp;amp;nbsp;Genome Research&#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &amp;amp;nbsp;2012/12/18&#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:hmorikawa@ifrec.osaka-u.ac.jp Hiromasa Morikawa] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: [https://fantom5-collaboration.gsc.riken.jp/wiki/index.php/File:Submit130114v3.docx Submit130114v3.docx]&#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF):&amp;amp;nbsp;[https://fantom5-collaboration.gsc.riken.jp/wiki/index.php/File:Submit130114v3.pdf Submit130114v3.pdf]&#039;&#039; &lt;br /&gt;
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== Title: An atlas of active enhancers across human cell types and tissues  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_35 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT NATURE&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; In higher organisms, cellular development and diversity is highly controlled by enhancers, which regulate the correct temporal and cell type-specific activation of gene expression. Despite their obvious importance for development and disease, the exact locations, target genes and mechanisms of enhancers are still poorly defined. Thus, there is an urgent need not only to identify enhancer locations, but also to elucidate their specific usage across the wide diversity of cells within the human body, their impact on regulation in healthy and diseased individuals, and how enhancers interact with target genes. Here, we use the FANTOM5 panel of tissue and primary cell samples covering the majority of human tissues and cell types to define an atlas of active, in vivo bidirectionally transcribed enhancers across the human body. It enables comparison of regulatory programs between different cells and tissues at unprecedented depth, and makes it possible to define distinct subsets of enhancers, including fetal-specific, cell-specific and ubiquitous enhancers – a novel enhancer subtype with distinct properties. We show that known target genes of enhancers can be recaptured using expression correlations and predict many novel enhancer-TSS associations. We present models confirming the utility of multiple redundant enhancers, which explain TSS expression strength rather than expression patterns. We demonstrate that disease-associated functional single nucleotide polymorphisms are over-represented in enhancers and that such enhancers often have disease-relevant expression patterns. The human enhancer atlas can be accessed through an online database and is a unique resource for studies on tissue/cell-specific enhancers and their gene interactions. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Robin Andersson1#, Claudia Gebhard2#, Irene Miguel-Escalada3, Ilka Hoof1, Xiaobei Zhao1, Christian Schmidl2, Eivind Valen1,4, Kang Li1, Lucia Schwarzfischer2, Dagmar Glatz2, Johanna Raithel2, Yun Chen1, Berit Lilje1, Nicolas Rapin1,5, Frederik Otzen Bagger1,5, Mette Jørgensen1, Mette Boyd1, Jette Bornholdt1, Kenneth Baillie6, Chris Mungall7, Timo Lassmann8, Hideya Kawaji8, Andreas Lennartsson9, Carsten Daub8,9, David Hume6, Peter Heutnik10, Alistair Forrest8, Piero Carninci8, Yoshihide Hayashizaki8, Ferenc Müller3, Michael Rehli2*, Albin Sandelin1* &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;RA, IH, EV, KL, YC, BL, XZ, MJ, HK, TL, KB, CM, NR, FOB, MR, AS made the computational analysis. TL, HK, CD, AF, PC, YH prepared, mapped and analyzed CAGE libraries. RA, CG, IH, EV, FM, PC, AF, AK, MB, JBL, AL, CD, DH, PH MR, AS interpreted results. CG, CS, ME, MR made the blood cell ChIP experiments, methylation assays and in vitro blood cell validations. IME, FM made zebrafish in vivo validations and interpretations. RA, CG, IH, FM, MR, AS wrote the paper. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks and raw CAGE mapped data from human, internal ChIP and other validation data &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; To be decided &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[robin@binf.ku.dk, michael.rehli@klinik.uni-regensburg.de, albin@binf.ku.dk , Michael Rehli Albin Sandelin] &amp;lt;br&amp;gt; &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] [[Image:Enhancerome full.pdf]]&#039;&#039;&#039; &lt;br /&gt;
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== Title: Analysis of DNA methylation and transcription during granulopoiesis reveals timed methylation changes in low CpG areas and regulation of transcription factor expression and motif activity  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_001 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT BLOOD&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;In development epigenetic mechanisms such as DNA methylation have been suggested to provide cellular memory to maintain pluripotency but also stabilize cell fate decisions and direct lineage restriction. In this study we set out to characterize changes in DNA methylation levels and gene expression during granulopoiesis using four distinct cell populations ranging from the oligopotent common myeloid progenitor stage to terminally differentiated neutrophils. We found a general decrease of DNA methylation during granulopoiesis. Methylation levels appear to change at specific differentiation stages and correlate with changes in transcription and motif activity of key hematopoietic transcription factors. Differentially methylated sites (DMSs) are preferentially located in areas distal to CpG islands and shores and are overrepresented in potentially regulatory enhancer elements. Overall this study depicts in detail the epigenetic and transcriptional changes that occur during granulopoiesis and supports the role of DNA methylation as a regulatory mechanism in cell differentiation. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Michelle Rönnerblad, Tor Olofsson, Sören Lehmann, RIKEN_OSC_members, Karl Ekwall*, Erik Arnér* &amp;amp;amp; Andreas Lennartsson* &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did most of the practical experiments, the bioinfo analysis (except CAGE related) and most manuscript writing, TO isolated the cells from bone marrows, SL gave valuable input to the planning, analysis and critically reviewed the manuscript, KE planned and supervised the study and contributed to the manuscript writing , EA supervised the bioinformatic analysis and performed the ones related to CAGE and contributed to the manuscript writing, AL initiated, planned and supervised the study and contributed to the manuscript writing and did some experiments. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on granulo precursor populations &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Blood &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;April 7th 2012 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:andreas.lennartsson@ki.se,Karl.Ekwall@ki.se,arner@gsc.riken.jp andreas lennartsson, Karl Ekwall, Erik Arner] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Rönnerblad.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Rönnerblad Aprl07.pdf]] &lt;br /&gt;
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== Title: Ceruloplasmin is a Novel Adipokine Which is Overexpressed in Adipose Tissue of Obese Subjects and in Obesity-Associated Cancer Cells  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_32 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT PLOS ONE&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; Obesity confers an increased risk of developing specific cancer forms. Although the mechanisms are unclear, increased fat cell secretion of specific proteins (adipokines) may promote/facilitate development of malignant tumors in obesity by cross-talk between adipose tissues and the tissues prone to develop cancer among obese. This was investigated using expression data from human adipose tissue of obese and non-obese as well as from a large panel of human cancer cell lines and corresponding primary cells and tissues. We identified three previously described adipokines, SERPINE1, SERPINE2 and C3 sharing a common cognate receptor LRP1 which was expressed in all cancer cell lines associated with obesity. Expression and secretion of SERPINE1 and C3 were increased in obese adipose tissue and their plasma levels were elevated in obese subjects. We also identified genes enriched in obesity-associated cancer cells compared to cell lines and corresponding healthy tissues or primary cells. We found expression of ceruloplasmin to be the most enriched in obesity-associated cancer cells. This gene was also significantly up-regulated in adipose tissue of obese subjects. Ceruloplasmin is the body’s main copper carrier and is involved in angiogenesis. We demonstrated that ceruloplasmin was a novel adipokine and that obese adipose tissue contributed markedly (22%) to the total protein level. In summary, we have identified several adipokines, which can serve as endocrine signals facilitating growth of obesity-associated cancer tumors. These adipocyte signals are increased in obesity and may be important for development of cancer associated with excess body fat. &lt;br /&gt;
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&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Erik Arner, Alistair Forrest, Anna Ehrlund, Niklas Mejhert, [Additional RIKEN people?], Jurga Laurencikiene, Mikael Rydén, Peter Arner &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s):&#039;&#039;&#039; Cancer Research &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:arner@gsc.riken.jp Erik Arner] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Fat cells and cancer draft 120816 EA.docx]] [[Image:Figs 2012-08-15.ppt]]&amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039; &lt;br /&gt;
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== Title: Interactive visualization and analysis of large-scale NGS data-sets using ZENBU  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_33 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: ACCEPTED AT NATURE BIOTECHNOLOGY&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039;The world of genome sciences has dramatically changed over the last 5 years. With the advent of next generation sequencers and RNA-expression sequencing, genome science is no longer the domain of a few elite centralized &amp;quot;genome centers&amp;quot; like in the early days of the field. The advance of next-generation sequencers has spurred an ever-growing body of tag-based data allowing the survey of chromatin states and transcriptome dynamics. Visualization of expression levels of genomic regions was achieved by displaying expression levels in various experimental conditions in dedicated tracks allowing investigators a direct comparison of their dynamics. Novel file formats and browser design have allowed for dealing efficiently with the depth of data produced by next-generation sequencer based technologies. Researchers need to interact within global collaborations and need easy ways to process, share and visualize their data in a secured manner prior to publication. To this end we have developed the ZENBU system. ZENBU is a web based system which is a social networking platform for secured data upload and data sharing with collaborators, a data processing system, and a visualization system. ZENBU provides the infrastructure for working with 100s of terrabytes of sequence data in the form of BAM sequence alignment files and genome annotation formats like BED and GFF, to efficiently cross-analyze these databsets using a Map-Reduce/autonomous-agent based parallel processing system, and provide fast efficient web services for user interfaces. The user interfaces for ZENBU is based on Web2.0 technologies in the form of a new expression-enhanced genome browser, and data manipulation interfaces for data upload, data processing, and data download. ZENBU currently contains the entire FANTOM 3/4/5 datasets, the entire ENCODE datasets, and much of the UCSC genome annotation data. ZENBU is planned to be a corner stone in the expanding global network of scientific sharing web systems.&amp;lt;br&amp;gt; &lt;br /&gt;
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&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Jessica Severin*, Marina Lizio, Jayson Harshbarger, Hideya Kawaji, Carsten Daub, The FANTOM5 consortium, Yoshihide Hayashizaki, Nicolas Bertin*, Alistair Forrest* &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement:&#039;&#039;&#039; &#039;&#039;JMS, ML, JH, HK, CD, YH, NB, AL&#039;&#039; &lt;br /&gt;
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*JMS, wrote the software/webservices. &lt;br /&gt;
*JMS, NB, planned the study. &lt;br /&gt;
*NB supervised the study. &lt;br /&gt;
*JMS, NB, contributed to the manuscript writing. &lt;br /&gt;
*JMS, NB, gave valuable input to the analysis in the manuscript. &lt;br /&gt;
*JMS, NB, critically reviewed the manuscript. &lt;br /&gt;
*&#039;&#039;[addition of any other, clearer or more precise statement is very welcome]&#039;&#039;&lt;br /&gt;
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&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s):&#039;&#039;&#039; Nature Biotech/Genome Research &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:severin@gsc.riken.jp,nbertin@gsc.riken.jp,forrest@gsc.riken.jp Jessica Severin, Nicolas Bertin, Alistair Forrest] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of the most up to date manuscript draft: &#039;&#039;&#039;[[Image:ZENBU manuscript.014 (1).docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Cell-type specificity and co-expression of regulatory polymorphisms associated with human disease  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_002 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO GENOME RESEARCH&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Our ability to use genetic associations with disease to develop better treatments has been limited by the difficulty of identifying a biological process, or cell type, on which to focus investigation. Most disease-associated polymorphisms do not lie within protein-coding genes, raising the possibility that variation in regulatory sequence plays a critical role in disease phenotypes. We have used genome-scale 5’RACE (CAGE) to identify the location and usage of transcription start sites in 864 human tissues, primary cells and cell lines, and show here that there is a strong enrichment for disease-associated variants within the sequence immediately adjacent to transcription start sites. Using the expression profiles of known variants associated with disease susceptibility, we identify experimentally-available cell types significantly associated with specific diseases and traits. The expression of genes known to be associated with particular diseases was positively correlated. Such co-expression was used to identify unreported candidate disease-associated regulatory regions within published genome-wide association studies (GWAS). The approach was validated by identifying candidate loci in a 2007 GWAS study that were subsequently validated in larger independent datasets These functional genomics approaches directly inform choices of model system and identify disease- and cell type-specific co-regulated networks for a wide range of common diseases. &lt;br /&gt;
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&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Baillie JK*, Haley CS, Schaefer U, Faulkner GJ, Freeman T, Brown JB, [others...], [Numerous RIKEN authors, order etc. TBC, at least including: Kawaji H, Forrest A, Carninci P]*, Hume DA* &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on Primary Cells &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Nature Genetics &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; ...&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:j.k.baillie@ed.ac.uk,david.hume@roslin.ed.ac.uk Kenneth Baillie, David Hume] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Ab Initio Prediction of Tissue-Specific Regulatory Modules in the FANTOM5 Project  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_005 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO GENOME RESEARCH&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;One of the major goals of the FANTOM5 project, the broadest TSS-based promoter-level expression atlas of transcriptional regulatory networks, is the identification of coding and non-coding, annotated and novel transcriptional units being transcribed in a cell-specific mode across the different biological states/samples. In this work we analyzed the FANTOM5 dataset using ScanAll, a newly developed software here described, to ab initio predict the presence of conserved elements in the genomic regions surrounding FANTOM5 promoters. Firstly we aimed at identifying motifs that were conserved in a subset of the selected genomic regions and that possibly corresponded to Transcription Factor Binding Sites (TFBS); we then expanded our analysis to pinpoint the existence of more complex, structured regulatory modules, that is groups of conserved motifs co-occurring in the aforementioned (co-expressed) regions within a fixed distance. We confirmed the sample-specificity of our output by showing that the majority of the obtained combinations of modules were able to divide the specimens into sample-specific groups, thus possibly explaining the peculiarities of regulatory events occurring in each tissue. Among these sites it was possible to confirm the presence of TFBS for known regulators already associated to those samples together with an additional and significant portion of motifs remaining unannotated, thus representing putative novel binding elements. In addition we were able to associate the presence of a significant portion of the identified motifs to distinct families of repeated elements, thus confirming a structural/functional feature of mammalian promoters that is currently emerging as one of the most peculiar regulatory aspects associated to mammalian phylogeny. Finally, we were able to identify previously uncharacterized aspects of the regulatory networks occurring in early-development samples thus confirming the significant advantage deriving from our modular approach. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Emiliano Dalla, Yari Ciani, Marco Zantoni, Alberto Policriti, Hideya Kawaji, Michiel J.L. de Hoon, Timo Lassmann, Alistair R.R. Forrest, Michael Rehli, Ivan Kulakovsky, Claudio Schneider, Silvano Piazza &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;ED conceived the project, developed part of the software, oversaw implementation, performed some of the analysis and most manuscript writing; YC implemented part of the software, performed some of the analysis and prepared some figures; MZ developed and implemented part of the software; AP developed part of the software and contributed to the manuscript writing; TL was responsible for tag mapping; HK managed the data handling; MR, IK and MJLdH were involved in motif assessment; ARRF was responsible for FANTOM5 management and concept; CS supervised the study; SP developed and implemented part of the software, carried out statistical tests and results interpretation and wrote parts of the manuscript. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on all of F5freeze1 &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;June 1st 2012; Update: December 21st 2012: Post Internal Review Update: January 28th 2012 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:emiliano.dalla@lncib.it Emiliano Dalla] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:FANTOM5 PromoteromeSatelliteLNCIB.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:FANTOM5 PromoteromeSatelliteLNCIB wFigures.pdf]] &lt;br /&gt;
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== Title: A high resolution spatial-temporal promoterome of the human brain (was Brain CAGE)  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_007 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO GENOME RESEARCH&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;The human brain is an extremely complex organ that governs our abilities for cognition, reasoning and emotions and is the control center for the body. Its morphology and functionality during development have been well studied, but the molecular mechanisms contributing to its function and maintenance later in life remain poorly understood. Complexity at the transcriptional level is likely to play a major role in defining its morphological and functional characteristics. To investigate this we used single molecule CAGE and created a high resolution atlas of transcription start sites for 15 anatomical regions of the human central nervous system, using post-mortem samples derived from infant and aged adult donors. On the transcriptional level brain is clearly distinguishable from other tissues even if we consider only non-coding genes or expression from genomic regions often described as genomic dark matter. Using these differences we identify a specific set of transcription start sites that characterizes the brain. We show extensive differences in transcription between infant and adult that in some cases can be linked to loci associated with major neurodegenerative diseases. The differential expression across distinct regions correlates well with developmentally and/or functionally related anatomical districts and is refelected by distinct networks of interacting transcription factors, a range of lncRNAs and novel transcripts co-expressed in a regionally biased manner. Overall we provide the scientific community with a powerful expression resource based on post-mortem tissue, particularly highlighting the contribution of non-coding RNAs to the transcriptional complexity of human central nervous system. &lt;br /&gt;
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&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Margherita Francescatto, Morana Vitezic, Patrizia Rizzu, Javier Simon-Sanchez, Robin Andersson, FANTOM5_RIKEN_OSC_members, Carsten O Daub, Albin Sandelin, MIchiel JL de Hoon, Piero Carninci, Alistair RR Forrest, Peter Heutink &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MF and MV did the analyses; MF, MV and PH wrote the manuscript, PR selected all samples, evaluated medical and pathological records and isolated RNA, JSS curated the list of disease loci, RA and AS provided the list of enhancers, ARRF, PC and PH designed the study ... &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on VUMC provided brain samples (adult and newborn); full list of samples presented in Supplementary Table 1&amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Genome Research &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Peter.Heutink@dzne.de,m.francescatto@vumc.nl,mvitezic@gsc.riken.jp Peter Heutink, Margherita Francescatto, Morana Vitezic] &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Final version: &#039;&#039;&#039;[[Image:Francescatto and Vitezic manuscript.pdf]] [[Image:Francescatto and Vitezic figures.pdf]] [[Image:Francescatto and Vitezic Supplementary Note.pdf]]&amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Chromatin states reveal functional associations for globally defined transcription start sites in four human cell lines  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_017&amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO BMC GENOMICS&#039;&#039;&#039; &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: Background: &#039;&#039;&#039;Deciphering the most common modes by which chromatin regulates transcription, and how this is related to cellular status and processes is an important task for improving our understanding of human cellular biology. The FANTOM5 and ENCODE projects represent two independent large scale efforts to map regulatory and transcriptional features to the human genome. Here we investigate chromatin features around a comprehensive set of transcription start sites in four cell lines by integrating data from these two projects. &#039;&#039;&#039;Results:&#039;&#039;&#039; Transcription start sites can be distinguished by chromatin states defined by specific combinations of both chromatin mark enrichment and the profile shapes of these chromatin marks. The observed patterns can be associated with cellular functions and processes, and they also show association with expression level, location relative to nearby genes, and CpG content. In particular we find a substantial number of repressed inter- and intra-genic transcription start sites enriched for active chromatin marks and Pol II, and these sites are strongly associated with immediate-early response processes and cell signaling. Associations between start sites with similar chromatin pattern are validated by significant correlations in their global expression profiles. &#039;&#039;&#039;Conclusions:&#039;&#039;&#039; The results confirm the link between chromatin state and cellular function, but they also show that the relationship between chromatin state and transcription is more subtle than previously appreciated. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Morten Rye, Geir Kjetil Sandve, Finn Drablos&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR, GKS and FD did data analysis and wrote the paper&amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE data, ENCODE chromatin ChIP-Seq and DNase HS data&amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Genome Biology &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;01.03.2013&amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:finn.drablos@ntnu.no,morten.rye@ntnu.no Finn Drablos,Morten Rye]&amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Internal submission draft FD GKS MBR 010313.docx]] &amp;lt;br&amp;gt; &#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Main figures 01032015.pdf]] &#039;&#039;&#039;Supplementary figures: &#039;&#039;&#039;[[Image:All supplem figs 01032013.pdf]] &lt;br /&gt;
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== Title: Evolution of expression patterns in human gene families illustrated by the FANTOM5-CAGE encyclopedia of transcription start sites.  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_019 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO BMC EVOLUTIONARY BIOLOGY&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &lt;br /&gt;
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Background Human gene families emerged through consecutive rounds of gene duplication. Here we apply the cutting-edge FANTOM5 single-nucleotide resolution atlas of transcription start sites from 1348 human and mouse libraries, to elucidate expression pattern evolution in animal gene families, with stress on comparison between human and mouse, and normal versus cancer cells. &lt;br /&gt;
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  Results  Broad over-view of FANTOM5 was obtained with intra-species and inter-species hierarchical clustering of human and mouse samples. In the follow-up, we dated gene duplications by phylogenetic timing, and investigated the rate of expression pattern divergence between duplicates, as well as the tissue-specificity of their expression. Finally, we defined the concept of phylo-expression signatures as strong associations between duplications of certain ages and expression samples in the FANTOM5 atlas. We show how phylo-expression signatures can be used to generate novel hypotheses on the nature of animal evolution, and discuss central nervous system and reproductive tract as two focused examples.   &lt;br /&gt;
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Conclusions A striking trend for young genes to be narrowly expressed was revealed. Several lines of evidence suggested that emergence of placental mammals was a unique period in the evolution of animal gene families and duplicates dating to that period have broader and more conserved expression patterns, with genes involved in chromatin assembly and epigenetic control driving the trend. A major strength of the FANTOM5 atlas is that it profiles normal tissues, primary cells, and cancer cell lines, and as expected, clustering of expression profiles showed a major divide between leukemias and solid tumors. Where the evolutionary link became apparent was that in cancer cell lines, unlike in tissues and primary cells, recent paralogs lacked the peak of highly correlated pairs. This novel finding suggests that global devolution and loss-of-evolutionary constraints on expression patterns accompany malignant transformation, and provides additional evidence in the debate on use of cancer cell lines as research models. &lt;br /&gt;
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&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;&amp;lt;br&amp;gt; OS and LH designed the study, performed all analyses, and wrote the manuscript. &amp;lt;br&amp;gt; A.R.R.F. and C.O.D were involved in the FANTOM5 concepts and management. &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE, TreeFam8&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Biology&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: November 30th&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Lukasz.Huminiecki@ki.se Lukasz Huminiecki] ,[mailto:oxana.sachenkova@scilifelab.se Oxana Sachenkova] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors&amp;amp;nbsp;: &#039;&#039;&#039;[[Image:The structure of animal expression pattern evolution.doc]] (only text)&amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:The structure of animal expression pattern evolution.pdf]] (this file includes all the figures) &lt;br /&gt;
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== Title:Automated clustering and quality control pipeline for CAGE technologies  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_030 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO BMC GENOMICS&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; To understand the manner and mechanisms of transcription initiation by RNA Polymerase II, different strategies for genome-wide detection of transcription start sites (TSSs) have been developed. We propose the clustering and quality control pipeline suitable for the Cap Analysis of Gene Expression (CAGE) sequence tags. The new framework uses parametric clustering at multiple scales and adopts the irreproducible discovery rate (IDR) to measure reproducibility between replicates of each cluster. Our pipeline reveals that genes have complicated structures of transcription initiation events and discover novel alternative promoters which were not detected by previous approaches. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039; Hiroko Ohmiya1, Morana Vitezic1, Martin Frith, Yoshihide Hayashizaki1, Timo Lassmann1 and many more &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:lassmann@gsc.riken.jp Timo Lassmann] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Manuscript Ohmiya Mar04.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Manuscript Ohmiya Mar04.pdf]] [[Image:Additional file2.txt]] &lt;br /&gt;
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== Title: Mesenchymal stem/stromal cells from high-grade serous ovarian cancer retain specific identity related to mesothelium  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_036 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO STEM CELLS&#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;The role of cancer microenvironment is being recognized as one of the critical hallmarks in both cancer progression and metastasis. Mesenchymal Stem/Stromal Cells (MSCs) are the precursors of various cell types that compose both normal and cancer tissue microenvironments. We have isolated MSCs from various High-Grade Serous Ovarian Carcinomas (HG-SOCs), demonstrated their normal genotype, and analyzed their transcriptome with respect to similarly derived normal tissues MSCs (N-MSCs), all embedded in the large comprehensive FANTOM5 sample dataset. An integrative analysis was conducted against the extensive panel of primary cells and tissues of the FANTOM5 project that allowed us to identify a cell-type specific transcriptional activity associated with the HG-SOC-MSCs. In fact the analysis shows that HG-SOC-MSCs retain a specific identity when compared to N-MSCs and are related to the primary mesothelial or mesothelial-derived cells representing the ovarian cellular precursors. Our results support the hypothesis that HG-SOC-MSCs are bona-fide representatives of the ovarian district thus tracing their origin either to the local mesothelium or highlighting the epigenetic conditioning of externally recruited MSCs by the HG-SOC cancer cell compartment. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Roberto Verardo, Silvano Piazza, Enio Klaric, Yari Ciani, Stefania Marzinotto, Laura Mariuzzi, Daniela Cesselli, Antonio P. Beltrami, Masayoshi Itoh, Hideya Kawaji, Timo Lassmann, Piero Carninci, Yoshihide Hayashizaki, Alistair R.R. Forrest, Carlo A. Beltrami, Claudio Schneider and the FANTOM consortium &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;R.V., S.P. and C.S. designed research and analyzed all the data; R.V. followed all sample RNA/DNA quality controls; S.P. designed software, carried out statistical tests and bioinformatics analysis; Y.C. implemented part of the software and prepared some figures; E.K. performed molecular biology assays; R.V., S.M., L.M., D.C., and A.P.B. performed cell isolation and characterization, R.V., D.C., A.P.B., C.A.B. and C.S. analyzed cell-biology data; M.I. was responsible for CAGE data production; T.L. was responsible for tag mapping; H.K. managed the data handling; P.C., Y.H. and A.R.R.F. were responsible for FANTOM5 management and concept; CS supervised the whole study; R.V., S.P. and C.S. wrote the manuscript. &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on all of F5freeze1 &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;October 15th 2012 &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:schneide@lncib.it Claudio Schneider] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Claudio.pdf]] &lt;br /&gt;
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== Title: A transient disruption of a fibroblast-specific transcriptional regulatory network potently promotes trans-differentiation  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_40&amp;lt;br&amp;gt; &#039;&#039;&#039;Status: SUBMITTED TO GENOME BIOLOGY &#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; Background: Transcriptional Regulatory Networks (TRN) coordinates multiple transcription factors (TF) in concert to maintain homeostasis and cellular function. The re-establishment of TRNs have been previously implicated in direct trans-differentiation studies where the newly introduced TFs switch-on a set of key regulatory factors to induce de novo expression and function. However, the extent to which TRNs in starting cell types, such as dermal fibroblasts, protect the cells from undergoing cellular reprogramming remains largely unexplored. Results: In order to identify specific TFs in fibroblasts, we first modeled the TRN of fibroblast cells using a Matrix-RNAi approach where 18 fibroblast-specific TFs were systematically knock-downed and profiled. The resulting expression matrix revealed 7 highly interconnected TFs as targetable factors. Interestingly, suppressing 4 out of 7 TFs generated lipid droplets and induced PPARG and CEBPA expression in the presence of adipocyte-inducing medium, while the control knockdown maintained fibroblastic characteristics in the same induction regime. The global gene expression analysis further revealed that the knockdown induced adipocytes (KDiADP) highly expressed genes associated with lipid metabolism and significantly suppressed fibroblast-specific genes. Conclusion: Overall, this study reveals the critical role of the TRN in protecting cells against aberrant reprogramming, and demonstrates, for the first time, the vulnerability of TRN, which may be a novel target to induce transgene-free trans-differentiations.  &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: Yasuhiro Tomaru, Ryota Hasegawa, Jay W. Shin , Takahiro Suzuki, Taiji Sato, Atsutaka Kubosaki, Masanori Suzuki, Yoshihide Hayashizaki and Harukazu Suzuki&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;YT designed and carried out experiments, analyzed and wrote the paper. RH carried out experiments, supported statistical analysis and wrote the paper. JS generated expression data, analyzed and wrote the paper. TS, TS and AK carried out validation of KDiADP cells. MS carried out editing of the manuscript. YH and HS coordinated all efforts and supervised the project&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Biology&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: May 20th, 2013&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:harukazu@gsc.riken.jp]Harukazu Suzuki, [mailto:jay.shin@gsc.riken.jp]Jay Shin&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:manuscript-YT-May17.docx]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Tomaru_F5_wiki.pdf]] &lt;br /&gt;
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== Title: Explaining the correlated properties of mammalian promoters  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_003 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Advanced draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;Proximal promoters are fundamental genomic elements for gene expression. They vary in terms of: GC percentage, CpG abundance, presence of TATA signal, evolutionary conservation, chromosomal spread of transcription start sites, and breadth of expression across cell types. These properties are correlated, and it has been suggested that there are two classes of promoter: one class with high CpG, widely spread transcription start sites, and broad expression, and another with TATA signals, narrow spread and restricted expression. It has been unclear, however, why these properties are correlated in this way. &lt;br /&gt;
&lt;br /&gt;
We re-examined these features using the deep FANTOM5 CAGE data from hundreds of cell types. Firstly, we point out subtle but important biases in previous definitions of promoters and of expression breadth. Secondly, we show that most promoters are rather non-specifically expressed across many cell types. Thirdly, promoters&#039; expression breadth is independent of maximum expression level, and therefore correlates with average expression level. Fourthly, the data show a more complex picture than two classes, with a network of direct and indirect correlations among promoter properties. By distinguishing the direct from the indirect correlations, we reveal simple explanations for them. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;M.C. Frith, ...? &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;All human and mouse Phase1 CTSSs &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Research(?) &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;Feb 2013 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:martin@cbrc.jp Martin Frith] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Mcf-prom-sat.pdf]] &amp;lt;br&amp;gt;&#039;&#039;&#039;Supplement: &#039;&#039;&#039;[[Image:Mcf-prom-sat-sup.pdf]] &lt;br /&gt;
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== Title: Homotypic clusters of transcription factor binding sites in the vicinity of transcription start sites  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_006 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Finished draft&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;Background&#039;&#039; &amp;lt;br&amp;gt;Transcription factors (TFs) specifically recognizing DNA binding sites (TFBS) play a key role in regulation of gene expression. Groups of closely localized TFBSs for a particular TF, so-called homotypic TFBS clusters (HCBSs), were originally detected in yeast and extensively studied in fruit fly early development. Recently HCs were found to be highly important for several human regulatory systems. &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;Motivation&#039;&#039; &amp;lt;br&amp;gt;It is a general practice to estimate an enrichment of binding sites in regulatory sequences. Still there is no systematized data whether the presence of HCBSs is common for promoter regions of human genes. The general properties of HCBSs also remain unclear as well as possible relation between HCBSs and regulation of tissue-specific expression. &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;Results&#039;&#039; &amp;lt;br&amp;gt;Using data on sample-specific transcription start sites (TSSs) detected in FANTOM5 and high quality binding models for more than 400 TFs from the HOCOMOCO TFBS model collection we have predicted TFBSs and corresponding HCBSs in promoter regions surrounding TSSs. TFBS models for most TFs were shown to form statistically significant HCBSs often formed by separate distant binding sites. For HCBSs of most of TFs we were able to identify samples having significant association between promoters of sample-specific or housekeeping TSSs. Thus for most of TFs we predict putative preferences for sample-specific or housekeeping HCBSs activity and provide a genome-wide map of HCBSs nearby FANTOM5-defined TSSs. &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;Supplementary information&#039;&#039; &amp;lt;br&amp;gt;https://fantom5-collaboration.gsc.riken.jp/webdav/home/vigg/homotypicus/ &lt;br /&gt;
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&#039;&#039;&#039;Authors: &#039;&#039;&#039;I.V. Kulakovskiy, Y.A. Medvedeva, M.S. Polishchuk, A.V. Favorov, S. Schmeier, T. Lassman, I.E. Vorontsov, RIKEN_OSC_members, V.J. Makeev &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039; IVK implemented the software and drafted the manuscript. YAM carried out statistical tests and results interpretation. MSP developed the homotypic cluster detection algorithm. AVF selected proper statistical tests. SS provided the housekeeping set of TSS-clusters. TL provided the set of sample-specific TSS-clusters. IEV estimated proper thresholds for PWMs used in the study. VJM coordinated the study. All the authors participated in writing and finalizing the manuscript. &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE - FANTOM5 FREEZE1, &amp;quot;robust&amp;quot; subset &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Nucleic Acids Research, Bioinformatics &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;18 June 2012 / Updated: 12 September 2012 / Minor fixes: 1 December 2012&amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:vsevolod.makeev@gmail.com,ivan.kulakovskiy@gmail.com Vsevolod Makeev, Ivan Kulakovskiy] &amp;lt;br&amp;gt; &lt;br /&gt;
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&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:HOMOTYPICUS-FANTOMsatellitepaper.r1.doc]] &amp;lt;br&amp;gt; &#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:HOMOTYPICUS-FANTOMsatellitepaper.r1.pdf]] &lt;br /&gt;
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== Title: Transcriptional profiling by deep CAGE of the human fibrillin/LTBP gene family, key regulators of mesenchymal cell functions.  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID&#039;&#039;&#039;: Phase1_014 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Good Draft &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; The fibrillins and latent transforming growth factor binding proteins (LTBPs) form a superfamily of extracellular matrix (ECM) proteins characterized by the presence of a unique domain, the 8-cysteine transforming growth factor beta (TGFβ) binding domain (TB domain). These proteins are involved in both maintaining the extracellular matrix and controlling the bioavailability of TGFβ family members. Genes encoding these proteins show differential expression in mesenchymal cell types which synthesise the extracellular matrix and form connective tissues. We have investigated the promoter regions of the seven gene family members using the FANTOM5 CAGE data base for human. Although the protein and nucleotide sequences show considerable homology, the promoter regions were quite diverse. The three fibrillin genes had a single predominant promoter cluster, while LTBP1 and LTBP4 showed promoter switching. Most of the family members were expressed in a range of mesenchymal and other cell types, often associated with use of alternative promoters or transcription start sites within a promoter. FBN3 was the lowest expressed gene, and was expressed only in embryonic and fetal tissues, primarily neurological. There was evidence of enhancer activity likely to be involved in expression of the genes. Each gene showed a unique pattern of transcription factor motifs or activity. This study highlights the role of alternative transcription start sites in regulating the tissue specificity of closely related genes and suggests that this important class of extracellular matrix genes is subject to subtle regulatory variations that explain the differential roles of members of this gene family.&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors:&#039;&#039;&#039; Margaret R Davis, RIKEN OSC members, Kim M Summers&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement:&#039;&#039;&#039; MRD performed the analysis and contributed to writing the paper, RIKEN OSC did ..., KMS performed the analysis and contributed to writing the paper&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used:&#039;&#039;&#039; Helicos CAGE on ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s):&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &amp;lt;br&amp;gt;Contact by email: &#039;&#039;&#039;[mailto:kim.summers@roslin.ed.ac.uk kim.summers@roslin.ed.ac.uk]&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors:&#039;&#039;&#039; [[File:Fantom5_FBN_paper_22-08-13.doc]], [[File:Supplementary_Table_1.pdf]], [[File:Supplementary_Table_2.xlsx]], [[File:Supplementary_Table_3.xlsx]], [[File:Supplementary_Table_4.xls]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF):&#039;&#039;&#039; [[Image:Fibrillin-LTBP satellite.pdf]]&amp;lt;br&amp;gt;&#039;&#039;&#039;Revised version of paper:&#039;&#039;&#039; &lt;br /&gt;
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[[Image:Summers Phase1 014 revision 18Apr2013.pdf]] &lt;br /&gt;
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== Title: Analysis of antisense transcription in loci associated to neurodegenerative diseases  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_022 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;The FANTOM5 sequencing datasets represent the largest collection of transcriptomes from human cell lines, primary cells and whole tissues of various origin. Transcription starting sites are mapped at high resolution by the use of a modified protocol of Cap-Analysis of Gene Expression (CAGE) for high-throughput single molecule next-generation sequencing with Helicos (hCAGE). We employed the FANTOM5 collection of data to address the role of antisense transcription in neurodegeneration. We focused our analysis exclusively on tissues and primary cells, to avoid artifacts due to cellular transformation in culture cell lines. Among the &amp;amp;gt;1261 human hCAGE libraries, we selected those of brain origin. Libraries from total blood and selected blood cell populations were also included in the analysis. A total of 66 tissue- and 244 cell-specific libraries were interrogated for the presence of antisense transcription to well-established loci associated to Alzheimer’s disease, Amyotrophic Lateral Sclerosis, Frontotemporal Dementia, Huntington’s and Parkinson’s disease. Almost all analyzed genes display some degree of antisense transcription mainly in their 5’ or 3’ UTRs. 5’ head-to-head divergent antisense transcription appears enriched compared to global distribution of sense/antisense pairs. Identified antisense transcripts may have coding and non-coding capabilities, with lncRNAs being more represented. Expressed transcripts are generally poorly annotated and may contain repetitive elements of the Alu, SINE and LINE families. Antisense transcription was validated for a subset of genes, including amyloid precursor protein, microtubule-associated protein tau, DJ-1, leucin-rich repeat kinase 2 and α-synuclein. The validated transcripts are predicted to have non-coding functions and most of them were not annotated. Quantitative analysis of antisense transcripts in human tissues indicates enrichment in the brain, compatible with FANTOM 5 data. Overall, these results represent the most comprehensive analysis of antisense transcription at loci associated to neurodegeneration and provide evidence for the existence of additional regulation of disease-related genes by previously not-annotated long non-coding RNAs. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Zucchelli SIlvia, Paolo Vatta, Stefania Fedele, Raffaella Calligaris, XXXX (from F5 consortium), Al Forrest, Piero Carninci and Stefano Gustincich &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;SZ designed the experiments, analyzed the data, wrote the manuscript; PV performed the bioinformatics analysis, prepared some figures; SF designed the experiments, performed the experiments and analyzed the data; RC provided reagents, designed the experiments and analyzed the experiments; SG analyzed the data, wrote the manuscript &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on human brain and blood samples&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Research, Plos Genetics, Human Molecular Genetics&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: beginning of june&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:gustinci@sissa.it,silvia.zucchelli@sissa.it Stefano Gustincich, Silvia Zucchelli] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Zucchelli FANTOM5 Manuscript 2013 01 22.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;&amp;lt;br&amp;gt;[[Image:Zucchelli FANTOM5 Figures 2013 01 22.pdf]]&amp;lt;br&amp;gt; [[Image:Zucchelli FANTOM5 Supplementary 2013 01 22.pdf]]&amp;lt;br&amp;gt;[[Image:Zucchelli FANTOM5 TAbles 2013 01 22.pdf]] &lt;br /&gt;
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== Title:Gateways to the promoter level mammalian expression atlas covering thousands of biological states in FANTOM5  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_025 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;working draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&amp;amp;nbsp;&#039;&#039;&#039;Monitoring RNA transcribed within a cell is an essential step toward the identification of active information within the genome, and the understanding the entire cellular system ultimately. Most previous studies involving the collection of a large set of genome-wide transcription profiles consist of tissues and/or cell lines. In the FANTOM5 (Functional ANnotation Of Mammals 5) project we monitored transcription in more than one thousand mammalian samples, including nearly two hundred primary cell types in human and more than one hundred cell types in mouse. We used a sequencing-based digital counting technology, CAGE (Cap Analysis Gene Expression), which skips any PCR amplification steps relying on a single molecule sequencer. &amp;amp;nbsp;This technology quantifies transcription starting site (TSS) activities at a single base pair resolution across the genomes, and the result is one of the largest sets of expression data available, consisting of diverse range of samples with a single platform based on the state-of-the-art technology. &lt;br /&gt;
&lt;br /&gt;
We assembled the FANTOM5 TSS profiles and subsequent analyses into a centralized data archive and set up various on-line resources available for the scientific community. Researchers in cell biology can easily search samples of interest to inspect active elements within a cell type. Researchers in molecular biology can search genes or transcription factors of interest to inspect in which biological context they are highly activated. Researchers in genome biology and other fields can explore the data within dynamic and interactive graphical user interfaces dedicated for genomic viewing and expression. We based all analysis and database systems on careful annotation of the diverse range of samples, including an application ontology consisting of cell types, anatomy, and diseases. This large set of expression data combined with the extensive and systematic sample annotation enables the scientific community to explore, examine, and slice the data from multiple aspects. Here we introduce the on-line resources and underlying data structure as well as discuss its potential impact in multiple research fields.&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;WP4, database providers, and analysis providers&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on phase1 freeze&amp;amp;nbsp;&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;package of word, pdf, etc: &#039;&#039;&#039;[[Image:130225-F5web-resource.zip]] &lt;br /&gt;
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== Title:Application of Semantic MediaWiki to snapshot of thousands of biological states in transcription  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_026 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Unknown&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;overview and instruction to the resource browser&#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: Shimoji H, Kawaji H., WP4 &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on phase1 freeze &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title:Identification of miRNA promoters and primary structures  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_028 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Unknown&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: ...&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: Kawaji H.&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Mogrify: Defining Factors For Direct Reprogramming Between All Cell Types  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_31 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft -&amp;amp;gt; PHASE2?&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &lt;br /&gt;
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We now know that cellular state is a plastic phenomenon which it is possible to control. There are an increasing number of reports in the literature of induced pluripotency and also induced trans-differentiated from one cell type to another. Each of these experiments has relied heavily on a process of trial and error as well as expert knowledge in order to discover the transcription factors capable of inducing a cell conversion. Here we present a novel network based method (Mogrify) that can identify the factors required for cell conversion. The method compares differences in expression, as measured by FANTOM5 CAGE data, over interaction networks. It provides candidate combinations of transcription factors for over-expression and knock-down, along with the likelihood score for conversion between any two given cell types. &lt;br /&gt;
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We show that the method reproduces known reprogramming factors for several successful trans-differentiations from the literature (eg between fibroblast and cardiomyocyte, neuron and hepatocyte); we discuss alternative combinations that Mogrify suggests for these conversions and for other conversions which have some experimental data in the literature but for which a fully successful differentiation is yet to be published. &lt;br /&gt;
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The technique is then run without human intervention on every possible pairwise combination of over 1000 libraries in the FANTOM 5 set, assessing possible combinations of factors for perturbation, and associating a likelihood score for success. This information is then used to construct a computational “Waddington landscape”, identifying the best candidate source and target cell types for future cell conversion experiments. This is the first resource of it’s kind, only made possible by the new FANTOM5 promoterome data and represents a considerable step forward in computational cell reprogramming. &lt;br /&gt;
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.&amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Owen and Julian &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks in all samples &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:owen.rackham@bristol.ac.uk,gough@cs.bris.ac.uk Owen Julian] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:Mogrify.pdf]] &lt;br /&gt;
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== Title: Investigating tissue-specificity of cancer-causing mutations  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_037 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; Over the past 10 years an increasing number of mutated genes have been associated with familial predisposition to cancer. Interestingly for more than half of these genes their involvement in cancer is restricted to only a few cancer types (e.g. BRCA1 mutations in breast and ovarian cancers). Even more interestingly some of these genes are expressed in all cell types, and perhaps we would expect to see them causing many more different types of cancer but they don’t. This paper will examine how these mutations are tolerated in most cell types but not in others by considering the network of genes expressed in different cell types and how that determines whether they are susceptible or resistant. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors: &#039;&#039;&#039;Jessica Mar, Daniel Carbajo, RIKEN_OSC_members, Alistair Forrest &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;JM and AF conceived the project, DC conducted the analyses. &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;&amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:jessica.mar@einstein.yu.edu Jessica Mar] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title:FANTOM5 reveals the genomic architecture of the genes implicated in Rett Syndrome  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_038 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Manuscript&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; Mutations in MECP2, FOXG1 and CDKL5 genes cause Rett Syndrome, a neuro-developmental disorder of the grey matter of the brain that almost exclusively affects females. We analyzed the RNA expression data from the FANTOM5 project in both human and mouse to investigate the genomic architecture of the three genes involved in Rett syndrome. Data from FANTOM 5 provides the unprecedented opportunity to study the expression profile, identify transcription start sites and, in conjunction with the recently released ENCODE dataset, identify the regulatory regions and transcription regulators of the three genes implicated in Rett Syndrome. Even though MECP2 and CDKL5 are expressed ubiquitously, mutations in these genes cause a brain specific phenotype suggesting that their role in brain is distinctly important from their function in other tissues. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors:&#039;&#039;&#039; Morana Vitezic, Leonard Lipovitch, Alistair RR Forrest, Piero Carninci, Alka Saxena &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; NAR &amp;lt;br&amp;gt; &#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; December 2012 &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:mvitezic@gmail.com,alka@gsc.riken.jp Morana Vitezic Alka Saxena] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:Rett paper.doc]] [[Image:Rett paper figures.zip]] [[Image:Rett paper supplementary.zip]]&amp;lt;br&amp;gt;&lt;br /&gt;
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== Title: Tissue gene expression profiles in relationship to primary cell gene expression profiles  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_039&amp;lt;br&amp;gt; &#039;&#039;&#039;Status:&#039;&#039;&#039; Initiated&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039; Gene expression profile in a particular tissue determines the functionalities and signature properties in contrast with other tissues within the same organism. It is uncertain whether gene expression profiles in tissues are simply the results of a combination of gene expressions of the group of constituting primary cells, or if gene expression profiles differ when primary cells have been isolated from the tissues. In this paper, we would like to investigate the gene expression profiles of primary cells in relationship to tissue expression profiles. We are interested in finding out what kind of genes are involved in the differences and what functions they might have. We aim to find out to what degree do tissues resemble the sum expression of its composing cells, and if there are genes that are expressed in a tissue environment only.&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Nancy Yu, Carsten Daub, possibly members from the Human Protein Atlas (HPA) group. &amp;lt;br&amp;gt; &#039;&#039;&#039;Authors contribution statement:&#039;&#039;&#039; NY will plan, perform most of the bioinformatics analyses and write the manuscript. CD will supervise the bioinformatics analysis, contribute additional ideas, and assist with manuscript writing. The HPA group will supply some data and possibly contribute to the bioinformatics analyses. &amp;lt;br&amp;gt; &#039;&#039;&#039;Datasets used:&#039;&#039;&#039; Phase1 CAGE peaks and possibly HPA RNA-Seq data&amp;lt;br&amp;gt; &#039;&#039;&#039;Target journal(s):&#039;&#039;&#039; Genome Research / PLoS Genetics / Genome Biology &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date:&#039;&#039;&#039; 2014 &amp;lt;br&amp;gt; &#039;&#039;&#039;Contact by email:&#039;&#039;&#039; [mailto:nancy.yu@ki.se,carsten.daub@ki.se Nancy Yu, Carsten Daub] &amp;lt;br&amp;gt; &#039;&#039;&#039;Word document version of manuscript for editors:&#039;&#039;&#039; [[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt; &#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF):&#039;&#039;&#039; [[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title:Pan Cancer Biomarkers and Disruption of Gene Regulatory Networks in Cancer.  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_41 &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract:&#039;&#039;&#039;CAGE FANTOM5 data collection of cancer cell lines and corresponding primary cells enables us to study the changes in transcription and gene regulation that occur in cancer and drive its development. CAGE is a 5’ sequence tag technology and provides us with a snapshot of genome-wide transcription start sites and shows in unbiased way which parts of genome are being actively transcribed into RNA in any given biological state. We analysed the CAGE data from 123 cell lines representing 12 different cancer types and compared them to the corresponding normal/primary cells (141 samples). We show the protein coding genes and non-coding RNAs that are up-regulated or down-regulated across multiple cancer types and therefore are candidates for pan cancer biomarkers. Furthermore, we show the changes in transcription factor activities and enhancer usage in cancers as well as disruption in gene co-regulation. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039;  Bogumil Kaczkowski, the FANTOM5 consortium and Alistair Forrest&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;  &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:forrest@gsc.riken.jp] &lt;br /&gt;
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== Title: Pathogen specific monocyte transcriptional responses  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_008 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Wells &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:c.wells@uq.edu.au,a.beckhouse@uq.edu.au Christine Wells, Anthony Beckhouse] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Promoter specificity in transcription determines cell lineage choice  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_018 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Delayed (as of September 12th)&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;This paper will use pathprint (pathway fingerprinting) to develop an overall phylogenetic tree of all samples in F5 freeze1. This tree will be used to determine relative ancestry of samples and cluster them accordingly. SwitchEngine will be run to find switching in TSS at key junctions in differentiation. Will show TSS dynamics at these informative sites is associated with lineage-commitment. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Emmanuel Dimont, Gabriel Altschuler, Winston Hide&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;ED did ..., GA did ..., WH did ...&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on all of F5freeze1 &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:edimont@hsph.harvard.edu,gabrielaltschuler@googlemail.com,whide@hsph.harvard.edu Winston Hide, Emmanuel Dimont, Gabriel Altschuler]&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Gene duplication and promoter divergence in mammals.  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_020&amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Delayed&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Lukasz Huminiecki and Core RIKEN Authors &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... and LH did everything else&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ..., F5 promoter and enhancer datasets, TreeFam8&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Research&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: September 1st&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Lukasz.Huminiecki@ki.se Lukasz Huminiecki] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Gene duplication and TF/miRNA regulatory network evolution in mammals.  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_021 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Delayed&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Lukasz Huminiecki and Core RIKEN Authors &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... and LH did everything else&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ... TreeFam8, miRBase, microRNA target predictions&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): Genome Research&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: December 1st&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Lukasz.Huminiecki@ki.se Lukasz Huminiecki] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Higher order chromatin structure and promoter activity  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_023 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Delayed -&amp;amp;gt; moved to PHASE2 &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Semple CA, Prendergast JG, et al &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: October 2012&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:Colin.Semple@igmm.ed.ac.uk,prenderj@gmail.com Colin Semple, James Prendergast] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title:Building context depending TSS regions from thousands of profiles  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_024 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Unknown&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039;about DPI &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Kawaji H, et al. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on phase1 freeze &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:kawaji@gsc.riken.jp KAWAJI Hideya] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Quantifying the informational complexity of transcriptional regulatory programmes  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_015 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;On-hold. Focussing on the biological results Phase1_016 rather than methods. Hope to return to methods later (phase2).&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; The regulation of gene expression defines cellular identity, it is the basis for organism development and it underlies many cellular responses to the environment. Its disruption is implicated in many diseases and changes in gene regulation appear to underlie many adaptations evident between species. Previously, genes have been grouped and interpreted based on their specificity of expression, for example house-keeping genes that are expressed by all cells in all conditions versus highly tissue restricted genes expressed by only one cell type at a particular developmental time. Although such studies have been informative they fail to capture important aspects of how a gene is regulated or account for the heterogeneous relatedness of samples. The expression pattern of a gene is the output of a regulatory program within the cell. A program that must affect many state changes (on, off, up, down) is likely to require more regulatory information (Kolmogorov complexity) than a program effecting fewer state switches. If we can quantify this &amp;quot;regulatory complexity&amp;quot; we can then start to address deeper questions as to where that regulatory information is encoded, how malleable it is through evolution and how susceptible it is to perturbation by mutation. For example, a greater regulatory complexity could correspond to a higher concentration of cis-regulatory sequences around the gene or alternatively a single binding site for a transcription factor that is the output of an extensive intracellular signalling network. To address these questions we have explored a range of possible measures regulatory complexity including distance weighted entropies, diversity and richness scores. This leads us to introduce a novel measure of regulatory complexity (CR). It is implemented as a hierarchical Baysian model parametrised through MCMC. The CR method can be thought of as a relative measure of the number of gene expression state changes occurring over a tree relating all analysed samples. A by-product of this analysis is a probabilistic scoring of gene expression state switches between all analysed gene expression libaries. CR is weighted to account for the genome wide similarity of gene expression between samples but does not depend on the inference of a fixed underlying tree topology. &amp;lt;font color=&amp;quot;green&amp;quot;&amp;gt;Note - this is intended as essentially a methods paper, see Phase1_016 for the biological insights paper&amp;lt;/font&amp;gt; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Sarah Baker, Martin Taylor &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;SB developed and implemented methods and performed general analyses; MT conceived the project and oversaw implementation and performed some of the analysis&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on primary cells from human and mouse.&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; Bioinformatics or Genome Research&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date:&#039;&#039;&#039; ETA July 2013 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:martin.tayor@igmm.ed.ac.uk,sarah.baker@igmm.ed.ac.uk Martin Taylor, Sarah Baker]&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Cis encoding of the master developmental regulatory programme  ==&lt;br /&gt;
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&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_016 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status: &#039;&#039;&#039;Working draft, starting dataset being regenerated to incorporate improved method&amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: &#039;&#039;&#039; The regulation of gene expression defines cellular identity, it is the basis for organism development and it underlies many cellular responses to the environment. Its disruption is implicated in many diseases and changes in gene regulation appear to underlie many adaptations evident between species. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors:&#039;&#039;&#039; Sarah Baker, Martin Taylor &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;SB developed and implemented methods and performed general analyses; MT conceived the project and oversaw implementation and performed some of the analysis&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;Helicos CAGE on primary cells from human and mouse. We may also want to use time course data for this paper (does that push it into phase2?).&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;PLoS Biology&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date:&#039;&#039;&#039; ETA March 2013 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:martin.tayor@igmm.ed.ac.uk,sarah.baker@igmm.ed.ac.uk Martin Taylor, Sarah Baker]&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
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== Title: Comparison of CAGE and RNA-Seq profiling results for human tissue and cell line data ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_042 &amp;lt;br&amp;gt; &#039;&#039;&#039;Status:&#039;&#039;&#039; Initiated&amp;lt;br&amp;gt;&#039;&#039;&#039;Abstract:&#039;&#039;&#039; A systematic comparison of CAGE and HPA RNA-Seq tissue and perhaps cell line dataset, since both datasets will probably serve as widely used gene expression resources for the research community. This study will inform the researchers of the features of each dataset, including consensus and individual strengths of each data source. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039; Nancy Yu, Carsten Daub, possibly members from the Human Protein Atlas (HPA) group. &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;NY will plan, perform most of the bioinformatics analyses and write the manuscript. CD will supervise the bioinformatics analysis, contribute additional ideas, and assist with manuscript writing. The HPA group will supply some data and possibly contribute to the bioinformatics analyses. &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039; phase1 CAGE peaks, HPA RNA-Seq data &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; early 2014 &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:nancy.yu@ki.se,carsten.daub@ki.se Nancy Yu, Carsten Daub] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
&lt;br /&gt;
----&lt;br /&gt;
&lt;br /&gt;
== Title:CAGExploreR: an R package for the analysis and visualization of promoter dynamics across multiple experiments  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID&#039;&#039;&#039;&#039;&#039;: &#039;&#039;Phase1_043 &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;NOTE:&#039;&#039;&amp;amp;nbsp;This is a paper describing what used to be called &amp;quot;SwitchEngine&amp;quot;&#039;&#039;&amp;lt;br&amp;gt;&#039;&#039;&#039;&#039;&#039;Status: &#039;&#039;&#039;Complete. Ready for Submission. &amp;lt;br&amp;gt;&#039;&#039;&#039;Abstract: &#039;&#039;&#039;Alternate promoter usage is an important molecular mechanism for generating RNA and protein diversity. Cap Analysis Gene Expression (CAGE) is a powerful approach for revealing the multiplicity of transcription start site (TSS) events across experiments and conditions. An understanding of the dynamics of TSS choice across these conditions requires both sensitive quantification and comparative visualization. We have developed CAGExploreR, an R package to detect and visualize changes in the utilization of specific TSS in wider promoter regions in the context of changes in overall gene expression when comparing different CAGE samples. These changes provide insight into the modification of transcript isoform gen-eration and associated regulatory network alterations associated with cell types and conditions. CAGExploreR is based on the FANTOM5 and MPromDb promoter set definitions but can also work with user-supplied regions. The package compares multiple CAGE libraries simultaneously and does not require replicates. Online supplementary materials describe methods in detail and a vignette demonstrates a workflow with a real data example.&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: &#039;&#039;&#039;Emmanuel Dimont, Alistair R. R. Forrest, Hideya Kawaji, Winston Hide and the&amp;amp;nbsp;FANTOM Consortium&amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;ED developed the method, the R package (software), wrote the paper and supplementary materials plus figures, AF created the original idea and provided data, HK created DPI TSS&amp;amp;nbsp;clusters (promoters), WH formulated the idea, wrote the paper and provided funding, FC provided funding and data.&amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 DPI clusters, ENCODE CAGE data for MCF7 and A549 cell lines&amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039;Bioinformatics&amp;amp;nbsp;(Application Note)&amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039;October 7th, 2013&amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;Emmanuel Dimont (edimont@mail.harvard.edu)&amp;amp;nbsp;&amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;The latest version of the manuscript, supplementary methods, R&amp;amp;nbsp;package and vignette can be found at [https://www.dropbox.com/sh/h9bf81ia56ywskq/gMPZ2KVfmi here].&amp;amp;nbsp;&amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;see above&#039;&#039;&#039;&amp;amp;nbsp;&#039;&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
----&lt;br /&gt;
&lt;br /&gt;
== Title:COPY THEN EDIT THIS TEMPLATE  ==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;ManuscriptID: &#039;&#039;&#039;Phase1_00x (INCREMENT THIS) &amp;lt;br&amp;gt; &#039;&#039;&#039;Abstract: ...&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors: R&#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Authors contribution statement: &#039;&#039;&#039;MR did ..., TO did ..., KE did ..., EA did ..., AL did ... &amp;lt;br&amp;gt;&#039;&#039;&#039;Datasets used: &#039;&#039;&#039;phase1 CAGE peaks &amp;lt;br&amp;gt;&#039;&#039;&#039;Target journal(s): &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Internal submission date: &#039;&#039;&#039; &amp;lt;br&amp;gt;&#039;&#039;&#039;Contact by email: &#039;&#039;&#039;[mailto:blah@change.this.edu,next.adress@change.this CHANGETHIScorresponding1 CHANGETHIScorresponding2] &amp;lt;br&amp;gt;&#039;&#039;&#039;Word document version of manuscript for editors: &#039;&#039;&#039;[[Image:XXXYOUR.doc]] &amp;lt;br&amp;gt;&#039;&#039;&#039;PDF version for general viewing (including all figs in one PDF): &#039;&#039;&#039;[[Image:XXXYOUR.pdf]] &lt;br /&gt;
&lt;br /&gt;
----&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=DNA_methylation_and_transcription&amp;diff=1667</id>
		<title>DNA methylation and transcription</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=DNA_methylation_and_transcription&amp;diff=1667"/>
		<updated>2011-03-04T15:00:49Z</updated>

		<summary type="html">&lt;p&gt;Yulia: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&#039;&#039;&#039; == DNA methylation affects TF binding and transcription == &#039;&#039;&#039;&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Introduction: It&#039;s commonly accepted that DNA methylation of a promoter repress transcription of this gene in normal tissues. Recently, a class of actively expressed genes having relatively methylated promoters has been discovered. &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Purpose&#039;&#039;&#039;: &lt;br /&gt;
&lt;br /&gt;
* To explore the idea that DNA methylation affects TFBS, preventing some TF from binding to DNA, and therefore represses transcription.&amp;lt;br&amp;gt;&lt;br /&gt;
* To select TFs most likely sensitive to DNA methylation (first, in human, possibly in other species)&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;We plan to do&#039;&#039;&#039;:&lt;br /&gt;
&lt;br /&gt;
1. Functional analysis&amp;lt;br&amp;gt;- Predict TFBS (homotypic clusters, composite elements?, conserved sites?) in promoters&amp;lt;br&amp;gt;- Estimate methylation level of each TFBS (may be, only core positions)&amp;lt;br&amp;gt;- Calculate correlation between level of methylation and expression from given promoter for each TFBS&amp;lt;br&amp;gt;- Select promoters and corresponding TFs with highest and lowest cc&lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;2. Evolutionary analysis&amp;lt;br&amp;gt;- Predict TFBS (homotypic clusters, composite elements?) in promoters&amp;lt;br&amp;gt;- For whole set of given TF&#039;s binding sites estimate probability of C&amp;amp;gt;T SNP (in CG or in CNG) and of C&amp;amp;gt;T interlineage substitution &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;We have data for functional analysis&#039;&#039;&#039;:&lt;br /&gt;
&lt;br /&gt;
Primary cells: &amp;lt;br&amp;gt;peripheral blood mononuclear cells PBMC (genome-wide BS-seq + CAGE)&amp;lt;br&amp;gt;&lt;br /&gt;
Tissues:&amp;lt;br&amp;gt;frontal cortex (genome-wide MeDIP-seq) - frontal lobe (CAGE)&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;We are looking for data&#039;&#039;&#039;:&lt;br /&gt;
DNA methylation with single bp resolution (genome-wide or covering not less then 1% of genome) in primary cells, tissues or cell lines represented in FANTOM5 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&#039;&#039;&#039;Collaboration&#039;&#039;&#039;: &lt;br /&gt;
Piotr (you are invited to add your plans of study on influence of TF on methylation) &lt;br /&gt;
&lt;br /&gt;
Sung-Joon Park (linear regression model for gene expression and methylation)&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;== TF binding affects DNA methylation == &#039;&#039;&#039; &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Collaborators are very welcome. If you have any ideas how to improve the research, please contact me directly or add your suggestion here. &amp;lt;br&amp;gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Task_assignments&amp;diff=1580</id>
		<title>Task assignments</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Task_assignments&amp;diff=1580"/>
		<updated>2011-03-03T09:15:58Z</updated>

		<summary type="html">&lt;p&gt;Yulia: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&#039;&#039;&#039;Task1: Sample acquisition/provision:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Al Forrest, Peter Klinken, Peter Heutink, Claudio Schneider, Kim Summers, Terry Meehan&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt; Sample list - text to Al ASAP&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &amp;amp;nbsp;1. List of missing cellular states on wiki – March 10&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &amp;amp;nbsp;2. Potential sources for missing states – March 10&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &amp;amp;nbsp;3. Acceptance of last snapshots for phase 1 – March 31 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task2: Sample Annotation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Terry Meehan, Win Hide, Tom Freeman, Al Forrest + sample providers&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt; Cell ontology mapping, Tissue ontology mapping&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp;&#039;&#039;Tom’s suggested Sample Annotation &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. UniqueID: Riken tracking number&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Unique_sample_name: Adult_liver.r1 , Tcell_HPC-induced_10h (preferably short, informed by Cell_Ontology)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Species: Hs., Mm., etc.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Sample_Class: Adult_tissue (AT.), Foetal_tissue (FT.), Primary_cell (PC.), Cell_culture (CC.), Time_course (TC-PC.), (TC-CC) etc.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Developmental stage: Adult, Foetal&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 6. Pathology: Normal, disease&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 7. Tissue: Liver, brain, heart etc&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 8. Cell_Ontology (maybe more than one level, to be used in primary sample ordering): Mesenchymal etc, etc&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 9. Cell_type: CO approved name e.g. Monocyte, Smooth_muscle, Intestinal_epithelium etc.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;10. Pertubation: LPS, HPC&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;11. Time: 0, 1h, 2h, 3h etc&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;12. Replicate: r1, r2, r3&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;13. Collection_method: FACS_sorting etc. with short description&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;14. Collection_method_reference: Pubmed_ID, web_address, protocol&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;15. Source: Roslin_Institute&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;16. Primary_contact: Joe_Bloggs&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;17. Email: joe.bloggs@roslin.ed.ac.uk&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;18. Tel: 0044 131 123 4567&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;19. Unique Donor ID&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Annotation of Data freeze 1 samples (cell, tissue – minimum to compare replicates)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Cell ontology – completion by March 15?&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Tissue ontology – March 15 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task3: Mapping:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Timo Lassmann, Geoff Faulkner&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; BAM&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; CTSS&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones: &amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Rescuing assessment (March 5)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Decision (March 7)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Genome version agreement – comment on pseudoautosomal regions&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Mapping of Data freeze 1 (GENAS??) &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task4: Tag clustering ( [[Working Group 1 - Tag clustering]]) &amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names: &amp;lt;/u&amp;gt;Piero Carninci, Cesare Furlanello, Piotr Balwierz, Martin Taylor, Martin Frith, Kawaji-san, Boris Lenhard, Albin Sandelin - clustering. David Hume, Ben Brown, Al Forrest - assessment&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Clusters defined as regions on a genome with strand, start, stop, peak and build(Bed?)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Intersect of the defined regions as an expression matrix/table across all samples (ie. intersect of clusters with expression in all libraries) &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Possibly.. intersected CTSS file of same regions to allow study of independent peak regulation&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Peak rec&amp;lt;br&amp;gt;&#039;&#039;&amp;amp;nbsp;Tom’s suggestion&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; Data Matrix Annotation&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; To be provided by Riken as raw counts (.raw) and tags per million (.tpm) but ultimately data may be normalised by other methods (.xxx)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. UniqueID: Gene Level (MGD, HGNC ID), Transcript or promoter level (ABC1.1, ABC1.2 etc), ncRNA (Leonard’s ID)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Class: Gene_promoter, ncRNA_promoter, other&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Chromosomal_location: e.g. alignment range, promoter peak&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Chromosome: Chr1&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Associated_seqs: refseq, ensembl_gene/transcript, ncRNA_ref&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 6. Other_associations: KEGG, GO etc&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;1. Agreement on format and training/tuning/assessment data and metrics (March 5)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;2. Competitive tracks available – March 25&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;3. Assessment – April 5&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;4. Run over paper 1 data freeze – mid April &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task5: State enriched(expression weighted) motif predictions (ab-initio and known): ([[Working Group 3 - Motifs and conservation]])&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt;Vlad Bajic, Michiel de Hoon, Boris Lenhard, Kenneth Baiulie, Timo Lassmann, Piotr Balwierz, Yulia Medvedeva&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats: &amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Ranked list of motifs enriched in each state for release 010&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Bed file(or similar) with actual predictions for release 010&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. As above on FREEZE 1 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task5: [[Tag Cluster Annotation]]:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Piero Carninci, Laurens Wilming, Timo Lassmann, Richard Baldarelli, Juha Kere, Leonard Lipovich(long ncRNA promoters, sense-antisense pair promoters, bidirectional promoters), Boris Lenhard(enhancers), Alison Meynert, Yulia Medvedeva (CpG islands, DNA methylation, Repeats)&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats: &amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Agreement on annotations to use (now?) (I will supply the global human lncRNAome and sense-antisense coordinates for the annotation. - LL)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Annotation of release 009 clusters using agreed strategy – available ASAP&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Annotation of data freeze 1 (ASAP after the clusters are provided) &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task6: Cross species promoter mapping:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Martin Taylor, Colin Semple, Vlad Bajic, Peter Heutink, Max Burroughs, Soichi Ogishima, Leonard Lipovich (if we are doing non-conserved promoters)&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&amp;amp;nbsp;&amp;amp;nbsp;Martins Taylor&#039;s suggested format&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_tag_cluster_ID &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_genome_assembly_ID&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_chrom &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_refPos &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_strand&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_tag_cluster_ID&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_genome_assembly_ID&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_chrom&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_refPos&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_strand&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projection_method (a list of rule sets whose criteria were met*)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projection_distance (a measure of confidence in the projection)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projection_result (e.g. species1_rescue, species2_rescue....)&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; *e.g. identical projected modal tag position, quantile overlap of&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projected tag cluster distributions, cluster coordinate overlap.&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Prediction/mapping of human promoters using mouse data (April 15)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Validation on the matched 10-30 human-mouse pairs (ie predict with mouse and check with actual human data). Assessment of strategy.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Prediction of human counterpart promoters for the rare mouse cells that we have collected (eg. intestinal stem cells, inner ear hair cells etc.). &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Do we need a preliminary count of nonconserved human promoters (those absent from the other 4 F5 species)? (LL)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task7: Expression visualization (gene level AND TSScluster level):&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Tom Freeman,Kenneth Baillie, Carsten Daub, Win Hide, Boris Lenhard, Albin Sandelin&amp;amp;nbsp;&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats&amp;lt;/u&amp;gt;: potential figures for displaying relationship of samples based on expression clustering&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Gene level information humanx3(tissue, cell line, primary cells) -&amp;amp;gt; Biolayout webstart&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Distance matrix, genes and pathways that separate each state - Win Hide &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task8: Promoter level expression analysis (differentially expressed genes/markers/transcription factors/ncRNAs):&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Piero Carninci, Al Forrest, Albin Sandelin, Vlad Bajic, Yulia Medvedeva, Hideya Kawaji, Ben Brown, Tom Freeman, Harukazu Suzuki, Colin Semple, David Human, Cesare Furlanello, Kenneth Bailie and Jess Mar, Timothy Ravasi, Leonard Lipovich&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;1. Agreement on metric for specificity/enrichment – entropy Ravasi March 5&amp;lt;br&amp;gt;2. Ranked list of most specific TFs for each state&amp;lt;br&amp;gt;3. Ranked list of ncRNAs specific for each state (incl. curated lncRNAs that define specific steady states -LL)&amp;lt;br&amp;gt;4. Ranked list of all genes specific for each state &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task9: Expression data mining:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Carlo, Tim&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt; &lt;br /&gt;
&lt;br /&gt;
1. Explore the data set using maximum curvilinearity methods and see if it helps classify the layers &lt;br /&gt;
&lt;br /&gt;
Boosting? SVMs? &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task10: Motif activity and TF expression integration (including deorphanization):&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Vlad Bajic, Michiel de Hoon, Piotr Balwierz, Yulia Medvedeva, Matthias Harbers, Al Forrest&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;1. Expanding Motifs&amp;lt;br&amp;gt;2. Core predicted set&amp;lt;br&amp;gt;3. Attempt at integrating list of sample enriched TFs and sample enriched motifs.&amp;lt;br&amp;gt;4. Prioritized orphan associations for validation &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task10:&amp;amp;nbsp;Sanity check:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Al Forrest, Piero Carninci&amp;lt;br&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;br&amp;gt;1. Assessment of strategy above&amp;lt;br&amp;gt;2. OK or repeat from step XYZ &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&#039;&#039;&#039;Task11: Data dissemination and nomenclature:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names: &amp;lt;/u&amp;gt;Win Hide, David Hume, Piero Carninci, Richard Baldarelli, Vlad Bajic, Tom Freeman, Yoshihide Hayashizaki, John Quackenbush, Laurens, Terry Meehan, Hideya Kawaji, Timo Lassmann, Albin Sandelin&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; ‘Promoter’ – dissemination&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; ‘expression’ – dissemination&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; ‘cell/sample’ – dissemination?&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Agreement on strategy&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Agreement on formats&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Agreement on third party data repositories (especially UCSC and Ensembl)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Core promoters with accessions and link to our data nomenclature &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task12: ChipSeq Validation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names&amp;lt;/u&amp;gt;: RIKEN OSC, Tim Ravasi, Al Forrest, Matthias Harbers, WP9&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Target selection – considering cell type, predictions, chip grade antibody, impact&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Assessment of targets&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Motif finding&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Public chip-seq data &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task13: Public data integration:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Vlad, David, Yulia, Louise, Thomas, Terry, Matthias &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Extract public Chip-seq data &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Extract public mouse KO &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Extract edges from literature mining (vlad) &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Extract in-situ mapping from Allen brain atlas, eurexpress, emage &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Extract localization information from human protein atlas&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task14: KDCAGE Validation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; RIKEN OSC, WP9 (intersection of chip-seq known and )&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Target selection – considering cell type, predictions, impact&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Assessment of targets&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Motif finding &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&#039;&#039;&#039;Task15: In-situ validation: (likely very late in project)&amp;lt;br&amp;gt;&#039;&#039;&#039;Committed names: Juha? Peter H? Silivia, &amp;lt;br&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; 1. Target selection &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; 2. In-situ on a small set of human samples&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; 3. Likely very late in the project&amp;lt;br&amp;gt; &amp;lt;br&amp;gt;&#039;&#039;&#039;Task16: Paper4 - Cross species network conservation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Al Forrest, Martin Taylor, Peter Heutink, Michiel de Hoon, Mamoon Rashid, Colin Semple, Vlad Bajic, Max Burroughs, Soichi Ogishima, Leonard Lipovich&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Gene level ortholog pairs (CDS matching)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. TSS cluster level ortholog pairs (genome matching)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Ortholog expression correlations (use expression data from above group, and ortholog mappings from 1 and 2)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. State specific motif enrichment (conservation independent)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Tf state specific expression&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 6. siRNA KD of SMC specific TFs in multiple species&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 7. Potential chip-seq&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 8. Availability of Macaque samples? Aortic SMC, hepatocytes, Bone marrow MSCs&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 9. Macrophages across all species? Peripheral blood (PBMCs)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 10. Integration of cis-networks (bidirectional promoters; TF to lncRNA; antisense lncRNA to sense mRNA gene) with existing networks -LL &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 11. Examples of specific non-conserved networks -LL &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&amp;lt;br&amp;gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Task_assignments&amp;diff=1579</id>
		<title>Task assignments</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Task_assignments&amp;diff=1579"/>
		<updated>2011-03-03T09:14:28Z</updated>

		<summary type="html">&lt;p&gt;Yulia: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&#039;&#039;&#039;Task1: Sample acquisition/provision:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Al Forrest, Peter Klinken, Peter Heutink, Claudio Schneider, Kim Summers, Terry Meehan&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt; Sample list - text to Al ASAP&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &amp;amp;nbsp;1. List of missing cellular states on wiki – March 10&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &amp;amp;nbsp;2. Potential sources for missing states – March 10&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &amp;amp;nbsp;3. Acceptance of last snapshots for phase 1 – March 31 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task2: Sample Annotation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Terry Meehan, Win Hide, Tom Freeman, Al Forrest + sample providers&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt; Cell ontology mapping, Tissue ontology mapping&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp;&#039;&#039;Tom’s suggested Sample Annotation &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. UniqueID: Riken tracking number&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Unique_sample_name: Adult_liver.r1 , Tcell_HPC-induced_10h (preferably short, informed by Cell_Ontology)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Species: Hs., Mm., etc.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Sample_Class: Adult_tissue (AT.), Foetal_tissue (FT.), Primary_cell (PC.), Cell_culture (CC.), Time_course (TC-PC.), (TC-CC) etc.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Developmental stage: Adult, Foetal&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 6. Pathology: Normal, disease&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 7. Tissue: Liver, brain, heart etc&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 8. Cell_Ontology (maybe more than one level, to be used in primary sample ordering): Mesenchymal etc, etc&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 9. Cell_type: CO approved name e.g. Monocyte, Smooth_muscle, Intestinal_epithelium etc.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;10. Pertubation: LPS, HPC&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;11. Time: 0, 1h, 2h, 3h etc&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;12. Replicate: r1, r2, r3&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;13. Collection_method: FACS_sorting etc. with short description&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;14. Collection_method_reference: Pubmed_ID, web_address, protocol&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;15. Source: Roslin_Institute&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;16. Primary_contact: Joe_Bloggs&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;17. Email: joe.bloggs@roslin.ed.ac.uk&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;18. Tel: 0044 131 123 4567&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;19. Unique Donor ID&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Annotation of Data freeze 1 samples (cell, tissue – minimum to compare replicates)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Cell ontology – completion by March 15?&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Tissue ontology – March 15 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task3: Mapping:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Timo Lassmann, Geoff Faulkner&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; BAM&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; CTSS&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones: &amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Rescuing assessment (March 5)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Decision (March 7)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Genome version agreement – comment on pseudoautosomal regions&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Mapping of Data freeze 1 (GENAS??) &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task4: Tag clustering ( [[Working Group 1 - Tag clustering]]) &amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names: &amp;lt;/u&amp;gt;Piero Carninci, Cesare Furlanello, Piotr Balwierz, Martin Taylor, Martin Frith, Kawaji-san, Boris Lenhard, Albin Sandelin - clustering. David Hume, Ben Brown, Al Forrest - assessment&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Clusters defined as regions on a genome with strand, start, stop, peak and build(Bed?)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Intersect of the defined regions as an expression matrix/table across all samples (ie. intersect of clusters with expression in all libraries) &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Possibly.. intersected CTSS file of same regions to allow study of independent peak regulation&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Peak rec&amp;lt;br&amp;gt;&#039;&#039;&amp;amp;nbsp;Tom’s suggestion&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; Data Matrix Annotation&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; To be provided by Riken as raw counts (.raw) and tags per million (.tpm) but ultimately data may be normalised by other methods (.xxx)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. UniqueID: Gene Level (MGD, HGNC ID), Transcript or promoter level (ABC1.1, ABC1.2 etc), ncRNA (Leonard’s ID)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Class: Gene_promoter, ncRNA_promoter, other&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Chromosomal_location: e.g. alignment range, promoter peak&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Chromosome: Chr1&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Associated_seqs: refseq, ensembl_gene/transcript, ncRNA_ref&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 6. Other_associations: KEGG, GO etc&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;1. Agreement on format and training/tuning/assessment data and metrics (March 5)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;2. Competitive tracks available – March 25&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;3. Assessment – April 5&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;4. Run over paper 1 data freeze – mid April &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task5: State enriched(expression weighted) motif predictions (ab-initio and known): ([[Working Group 3 - Motifs and conservation]])&lt;br /&gt;
&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt;Vlad Bajic, Michiel de Hoon, Boris Lenhard, Kenneth Baiulie, Timo Lassmann, Piotr Balwierz, Yulia Medvedeva&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats: &amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Ranked list of motifs enriched in each state for release 010&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Bed file(or similar) with actual predictions for release 010&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. As above on FREEZE 1 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task5: [[Tag Cluster Annotation]]:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Piero Carninci, Laurens Wilming, Timo Lassmann, Richard Baldarelli, Juha Kere, Leonard Lipovich(long ncRNA promoters, sense-antisense pair promoters, bidirectional promoters), Boris Lenhard(enhancers), Alison Meynert, Yulia Medvedeva (CpG islands, DNA methylation, Repeats)&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats: &amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Agreement on annotations to use (now?) (I will supply the global human lncRNAome and sense-antisense coordinates for the annotation. - LL)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Annotation of release 009 clusters using agreed strategy – available ASAP&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Annotation of data freeze 1 (ASAP after the clusters are provided) &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task6: Cross species promoter mapping:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Martin Taylor, Colin Semple, Vlad Bajic, Peter Heutink, Max Burroughs, Soichi Ogishima, Leonard Lipovich (if we are doing non-conserved promoters)&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&amp;amp;nbsp;&amp;amp;nbsp;Martins Taylor&#039;s suggested format&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_tag_cluster_ID &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_genome_assembly_ID&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_chrom &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_refPos &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_strand&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_tag_cluster_ID&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_genome_assembly_ID&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_chrom&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_refPos&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_strand&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projection_method (a list of rule sets whose criteria were met*)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projection_distance (a measure of confidence in the projection)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projection_result (e.g. species1_rescue, species2_rescue....)&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; *e.g. identical projected modal tag position, quantile overlap of&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projected tag cluster distributions, cluster coordinate overlap.&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Prediction/mapping of human promoters using mouse data (April 15)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Validation on the matched 10-30 human-mouse pairs (ie predict with mouse and check with actual human data). Assessment of strategy.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Prediction of human counterpart promoters for the rare mouse cells that we have collected (eg. intestinal stem cells, inner ear hair cells etc.). &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Do we need a preliminary count of nonconserved human promoters (those absent from the other 4 F5 species)? (LL)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task7: Expression visualization (gene level AND TSScluster level):&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Tom Freeman,Kenneth Baillie, Carsten Daub, Win Hide, Boris Lenhard, Albin Sandelin&amp;amp;nbsp;&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats&amp;lt;/u&amp;gt;: potential figures for displaying relationship of samples based on expression clustering&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Gene level information humanx3(tissue, cell line, primary cells) -&amp;amp;gt; Biolayout webstart&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Distance matrix, genes and pathways that separate each state - Win Hide &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task8: Promoter level expression analysis (differentially expressed genes/markers/transcription factors/ncRNAs):&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Piero Carninci, Al Forrest, Albin Sandelin, Vlad Bajic, Yulia Medvedeva, Hideya Kawaji, Ben Brown, Tom Freeman, Harukazu Suzuki, Colin Semple, David Human, Cesare Furlanello, Kenneth Bailie and Jess Mar, Timothy Ravasi, Leonard Lipovich&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;1. Agreement on metric for specificity/enrichment – entropy Ravasi March 5&amp;lt;br&amp;gt;2. Ranked list of most specific TFs for each state&amp;lt;br&amp;gt;3. Ranked list of ncRNAs specific for each state (incl. curated lncRNAs that define specific steady states -LL)&amp;lt;br&amp;gt;4. Ranked list of all genes specific for each state &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task9: Expression data mining:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Carlo, Tim&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt; &lt;br /&gt;
&lt;br /&gt;
1. Explore the data set using maximum curvilinearity methods and see if it helps classify the layers &lt;br /&gt;
&lt;br /&gt;
Boosting? SVMs? &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task10: Motif activity and TF expression integration (including deorphanization):&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Vlad Bajic, Michiel de Hoon, Piotr Balwierz, Yulia Medvedeva, Matthias Harbers, Al Forrest&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;1. Expanding Motifs&amp;lt;br&amp;gt;2. Core predicted set&amp;lt;br&amp;gt;3. Attempt at integrating list of sample enriched TFs and sample enriched motifs.&amp;lt;br&amp;gt;4. Prioritized orphan associations for validation &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task10:&amp;amp;nbsp;Sanity check:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Al Forrest, Piero Carninci&amp;lt;br&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;br&amp;gt;1. Assessment of strategy above&amp;lt;br&amp;gt;2. OK or repeat from step XYZ &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&#039;&#039;&#039;Task11: Data dissemination and nomenclature:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names: &amp;lt;/u&amp;gt;Win Hide, David Hume, Piero Carninci, Richard Baldarelli, Vlad Bajic, Tom Freeman, Yoshihide Hayashizaki, John Quackenbush, Laurens, Terry Meehan, Hideya Kawaji, Timo Lassmann, Albin Sandelin&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; ‘Promoter’ – dissemination&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; ‘expression’ – dissemination&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; ‘cell/sample’ – dissemination?&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Agreement on strategy&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Agreement on formats&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Agreement on third party data repositories (especially UCSC and Ensembl)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Core promoters with accessions and link to our data nomenclature &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task12: ChipSeq Validation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names&amp;lt;/u&amp;gt;: RIKEN OSC, Tim Ravasi, Al Forrest, Matthias Harbers, WP9&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Target selection – considering cell type, predictions, chip grade antibody, impact&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Assessment of targets&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Motif finding&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Public chip-seq data &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task13: Public data integration:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Vlad, David, Yulia, Louise, Thomas, Terry, Matthias &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Extract public Chip-seq data &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Extract public mouse KO &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Extract edges from literature mining (vlad) &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Extract in-situ mapping from Allen brain atlas, eurexpress, emage &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Extract localization information from human protein atlas&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task14: KDCAGE Validation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; RIKEN OSC, WP9 (intersection of chip-seq known and )&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Target selection – considering cell type, predictions, impact&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Assessment of targets&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Motif finding &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&#039;&#039;&#039;Task15: In-situ validation: (likely very late in project)&amp;lt;br&amp;gt;&#039;&#039;&#039;Committed names: Juha? Peter H? Silivia, &amp;lt;br&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; 1. Target selection &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; 2. In-situ on a small set of human samples&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; 3. Likely very late in the project&amp;lt;br&amp;gt; &amp;lt;br&amp;gt;&#039;&#039;&#039;Task16: Paper4 - Cross species network conservation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Al Forrest, Martin Taylor, Peter Heutink, Michiel de Hoon, Mamoon Rashid, Colin Semple, Vlad Bajic, Max Burroughs, Soichi Ogishima, Leonard Lipovich&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Gene level ortholog pairs (CDS matching)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. TSS cluster level ortholog pairs (genome matching)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Ortholog expression correlations (use expression data from above group, and ortholog mappings from 1 and 2)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. State specific motif enrichment (conservation independent)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Tf state specific expression&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 6. siRNA KD of SMC specific TFs in multiple species&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 7. Potential chip-seq&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 8. Availability of Macaque samples? Aortic SMC, hepatocytes, Bone marrow MSCs&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 9. Macrophages across all species? Peripheral blood (PBMCs)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 10. Integration of cis-networks (bidirectional promoters; TF to lncRNA; antisense lncRNA to sense mRNA gene) with existing networks -LL &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 11. Examples of specific non-conserved networks -LL &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&amp;lt;br&amp;gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Task_assignments&amp;diff=1578</id>
		<title>Task assignments</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Task_assignments&amp;diff=1578"/>
		<updated>2011-03-03T09:12:13Z</updated>

		<summary type="html">&lt;p&gt;Yulia: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&#039;&#039;&#039;Task1: Sample acquisition/provision:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Al Forrest, Peter Klinken, Peter Heutink, Claudio Schneider, Kim Summers, Terry Meehan&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt; Sample list - text to Al ASAP&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &amp;amp;nbsp;1. List of missing cellular states on wiki – March 10&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &amp;amp;nbsp;2. Potential sources for missing states – March 10&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &amp;amp;nbsp;3. Acceptance of last snapshots for phase 1 – March 31 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task2: Sample Annotation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Terry Meehan, Win Hide, Tom Freeman, Al Forrest + sample providers&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt; Cell ontology mapping, Tissue ontology mapping&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp;&#039;&#039;Tom’s suggested Sample Annotation &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. UniqueID: Riken tracking number&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Unique_sample_name: Adult_liver.r1 , Tcell_HPC-induced_10h (preferably short, informed by Cell_Ontology)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Species: Hs., Mm., etc.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Sample_Class: Adult_tissue (AT.), Foetal_tissue (FT.), Primary_cell (PC.), Cell_culture (CC.), Time_course (TC-PC.), (TC-CC) etc.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Developmental stage: Adult, Foetal&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 6. Pathology: Normal, disease&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 7. Tissue: Liver, brain, heart etc&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 8. Cell_Ontology (maybe more than one level, to be used in primary sample ordering): Mesenchymal etc, etc&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 9. Cell_type: CO approved name e.g. Monocyte, Smooth_muscle, Intestinal_epithelium etc.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;10. Pertubation: LPS, HPC&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;11. Time: 0, 1h, 2h, 3h etc&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;12. Replicate: r1, r2, r3&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;13. Collection_method: FACS_sorting etc. with short description&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;14. Collection_method_reference: Pubmed_ID, web_address, protocol&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;15. Source: Roslin_Institute&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;16. Primary_contact: Joe_Bloggs&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;17. Email: joe.bloggs@roslin.ed.ac.uk&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;18. Tel: 0044 131 123 4567&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;19. Unique Donor ID&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Annotation of Data freeze 1 samples (cell, tissue – minimum to compare replicates)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Cell ontology – completion by March 15?&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Tissue ontology – March 15 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task3: Mapping:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Timo Lassmann, Geoff Faulkner&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; BAM&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; CTSS&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones: &amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Rescuing assessment (March 5)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Decision (March 7)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Genome version agreement – comment on pseudoautosomal regions&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Mapping of Data freeze 1 (GENAS??) &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task4: Tag clustering ( [[Working Group 1 - Tag clustering]]) &amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names: &amp;lt;/u&amp;gt;Piero Carninci, Cesare Furlanello, Piotr Balwierz, Martin Taylor, Martin Frith, Kawaji-san, Boris Lenhard, Albin Sandelin - clustering. David Hume, Ben Brown, Al Forrest - assessment&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Clusters defined as regions on a genome with strand, start, stop, peak and build(Bed?)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Intersect of the defined regions as an expression matrix/table across all samples (ie. intersect of clusters with expression in all libraries) &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Possibly.. intersected CTSS file of same regions to allow study of independent peak regulation&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Peak rec&amp;lt;br&amp;gt;&#039;&#039;&amp;amp;nbsp;Tom’s suggestion&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; Data Matrix Annotation&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; To be provided by Riken as raw counts (.raw) and tags per million (.tpm) but ultimately data may be normalised by other methods (.xxx)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. UniqueID: Gene Level (MGD, HGNC ID), Transcript or promoter level (ABC1.1, ABC1.2 etc), ncRNA (Leonard’s ID)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Class: Gene_promoter, ncRNA_promoter, other&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Chromosomal_location: e.g. alignment range, promoter peak&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Chromosome: Chr1&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Associated_seqs: refseq, ensembl_gene/transcript, ncRNA_ref&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 6. Other_associations: KEGG, GO etc&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;1. Agreement on format and training/tuning/assessment data and metrics (March 5)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;2. Competitive tracks available – March 25&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;3. Assessment – April 5&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;4. Run over paper 1 data freeze – mid April &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task5: State enriched(expression weighted) motif predictions (ab-initio and known): [[Working_Group_3_-_Motifs_and_conservation]]&lt;br /&gt;
&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt;Vlad Bajic, Michiel de Hoon, Boris Lenhard, Kenneth Baiulie, Timo Lassmann, Piotr Balwierz, Yulia Medvedeva&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats: &amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Ranked list of motifs enriched in each state for release 010&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Bed file(or similar) with actual predictions for release 010&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. As above on FREEZE 1 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task5: [[Tag Cluster Annotation]]:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Piero Carninci, Laurens Wilming, Timo Lassmann, Richard Baldarelli, Juha Kere, Leonard Lipovich(long ncRNA promoters, sense-antisense pair promoters, bidirectional promoters), Boris Lenhard(enhancers), Alison Meynert, Yulia Medvedeva (CpG islands, DNA methylation, Repeats)&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats: &amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Agreement on annotations to use (now?) (I will supply the global human lncRNAome and sense-antisense coordinates for the annotation. - LL)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Annotation of release 009 clusters using agreed strategy – available ASAP&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Annotation of data freeze 1 (ASAP after the clusters are provided) &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task6: Cross species promoter mapping:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Martin Taylor, Colin Semple, Vlad Bajic, Peter Heutink, Max Burroughs, Soichi Ogishima, Leonard Lipovich (if we are doing non-conserved promoters)&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&amp;amp;nbsp;&amp;amp;nbsp;Martins Taylor&#039;s suggested format&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_tag_cluster_ID &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_genome_assembly_ID&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_chrom &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_refPos &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_strand&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_tag_cluster_ID&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_genome_assembly_ID&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_chrom&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_refPos&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_strand&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projection_method (a list of rule sets whose criteria were met*)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projection_distance (a measure of confidence in the projection)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projection_result (e.g. species1_rescue, species2_rescue....)&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; *e.g. identical projected modal tag position, quantile overlap of&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projected tag cluster distributions, cluster coordinate overlap.&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Prediction/mapping of human promoters using mouse data (April 15)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Validation on the matched 10-30 human-mouse pairs (ie predict with mouse and check with actual human data). Assessment of strategy.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Prediction of human counterpart promoters for the rare mouse cells that we have collected (eg. intestinal stem cells, inner ear hair cells etc.). &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Do we need a preliminary count of nonconserved human promoters (those absent from the other 4 F5 species)? (LL)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task7: Expression visualization (gene level AND TSScluster level):&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Tom Freeman,Kenneth Baillie, Carsten Daub, Win Hide, Boris Lenhard, Albin Sandelin&amp;amp;nbsp;&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats&amp;lt;/u&amp;gt;: potential figures for displaying relationship of samples based on expression clustering&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Gene level information humanx3(tissue, cell line, primary cells) -&amp;amp;gt; Biolayout webstart&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Distance matrix, genes and pathways that separate each state - Win Hide &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task8: Promoter level expression analysis (differentially expressed genes/markers/transcription factors/ncRNAs):&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Piero Carninci, Al Forrest, Albin Sandelin, Vlad Bajic, Yulia Medvedeva, Hideya Kawaji, Ben Brown, Tom Freeman, Harukazu Suzuki, Colin Semple, David Human, Cesare Furlanello, Kenneth Bailie and Jess Mar, Timothy Ravasi, Leonard Lipovich&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;1. Agreement on metric for specificity/enrichment – entropy Ravasi March 5&amp;lt;br&amp;gt;2. Ranked list of most specific TFs for each state&amp;lt;br&amp;gt;3. Ranked list of ncRNAs specific for each state (incl. curated lncRNAs that define specific steady states -LL)&amp;lt;br&amp;gt;4. Ranked list of all genes specific for each state &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task9: Expression data mining:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Carlo, Tim&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt; &lt;br /&gt;
&lt;br /&gt;
1. Explore the data set using maximum curvilinearity methods and see if it helps classify the layers &lt;br /&gt;
&lt;br /&gt;
Boosting? SVMs? &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task10: Motif activity and TF expression integration (including deorphanization):&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Vlad Bajic, Michiel de Hoon, Piotr Balwierz, Yulia Medvedeva, Matthias Harbers, Al Forrest&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;1. Expanding Motifs&amp;lt;br&amp;gt;2. Core predicted set&amp;lt;br&amp;gt;3. Attempt at integrating list of sample enriched TFs and sample enriched motifs.&amp;lt;br&amp;gt;4. Prioritized orphan associations for validation &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task10:&amp;amp;nbsp;Sanity check:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Al Forrest, Piero Carninci&amp;lt;br&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;br&amp;gt;1. Assessment of strategy above&amp;lt;br&amp;gt;2. OK or repeat from step XYZ &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&#039;&#039;&#039;Task11: Data dissemination and nomenclature:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names: &amp;lt;/u&amp;gt;Win Hide, David Hume, Piero Carninci, Richard Baldarelli, Vlad Bajic, Tom Freeman, Yoshihide Hayashizaki, John Quackenbush, Laurens, Terry Meehan, Hideya Kawaji, Timo Lassmann, Albin Sandelin&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; ‘Promoter’ – dissemination&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; ‘expression’ – dissemination&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; ‘cell/sample’ – dissemination?&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Agreement on strategy&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Agreement on formats&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Agreement on third party data repositories (especially UCSC and Ensembl)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Core promoters with accessions and link to our data nomenclature &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task12: ChipSeq Validation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names&amp;lt;/u&amp;gt;: RIKEN OSC, Tim Ravasi, Al Forrest, Matthias Harbers, WP9&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Target selection – considering cell type, predictions, chip grade antibody, impact&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Assessment of targets&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Motif finding&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Public chip-seq data &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task13: Public data integration:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Vlad, David, Yulia, Louise, Thomas, Terry, Matthias &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Extract public Chip-seq data &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Extract public mouse KO &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Extract edges from literature mining (vlad) &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Extract in-situ mapping from Allen brain atlas, eurexpress, emage &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Extract localization information from human protein atlas&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task14: KDCAGE Validation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; RIKEN OSC, WP9 (intersection of chip-seq known and )&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Target selection – considering cell type, predictions, impact&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Assessment of targets&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Motif finding &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&#039;&#039;&#039;Task15: In-situ validation: (likely very late in project)&amp;lt;br&amp;gt;&#039;&#039;&#039;Committed names: Juha? Peter H? Silivia, &amp;lt;br&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; 1. Target selection &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; 2. In-situ on a small set of human samples&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; 3. Likely very late in the project&amp;lt;br&amp;gt; &amp;lt;br&amp;gt;&#039;&#039;&#039;Task16: Paper4 - Cross species network conservation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Al Forrest, Martin Taylor, Peter Heutink, Michiel de Hoon, Mamoon Rashid, Colin Semple, Vlad Bajic, Max Burroughs, Soichi Ogishima, Leonard Lipovich&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Gene level ortholog pairs (CDS matching)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. TSS cluster level ortholog pairs (genome matching)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Ortholog expression correlations (use expression data from above group, and ortholog mappings from 1 and 2)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. State specific motif enrichment (conservation independent)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Tf state specific expression&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 6. siRNA KD of SMC specific TFs in multiple species&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 7. Potential chip-seq&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 8. Availability of Macaque samples? Aortic SMC, hepatocytes, Bone marrow MSCs&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 9. Macrophages across all species? Peripheral blood (PBMCs)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 10. Integration of cis-networks (bidirectional promoters; TF to lncRNA; antisense lncRNA to sense mRNA gene) with existing networks -LL &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 11. Examples of specific non-conserved networks -LL &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&amp;lt;br&amp;gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=DNA_methylation_and_transcription&amp;diff=1563</id>
		<title>DNA methylation and transcription</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=DNA_methylation_and_transcription&amp;diff=1563"/>
		<updated>2011-03-03T08:00:12Z</updated>

		<summary type="html">&lt;p&gt;Yulia: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&#039;&#039;&#039; == DNA methylation affects TF binding and transcription == &#039;&#039;&#039;&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Introduction: It&#039;s commonly accepted that DNA methylation of a promoter repress transcription of this gene in normal tissues. Recently, a class of actively expressed genes having relatively methylated promoters has been discovered. &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Our purposes&#039;&#039;&#039;: &lt;br /&gt;
&lt;br /&gt;
* To explore the idea that DNA methylation affects TFBS, preventing some TF from binding to DNA, and therefore represses transcription.&amp;lt;br&amp;gt;&lt;br /&gt;
* To select TFs most likely sensitive to DNA methylation (first, in human, mb in other spicies later)&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;We plan to do&#039;&#039;&#039;:&lt;br /&gt;
&lt;br /&gt;
1. Functional analysis&amp;lt;br&amp;gt;- Predict TFBS (TFBS clusters?) in promoters&amp;lt;br&amp;gt;- Estimate methylation level of each TFBS (may be, only core positions of TFBS)&amp;lt;br&amp;gt;- Calculate correlation between level of methylation and expression from given promoter for each TFBS&amp;lt;br&amp;gt;- Select lists of TFs with highest and lowest cc&lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;2. Evolutionary analysis&amp;lt;br&amp;gt;- Predict TFBS (TFBS clusters?) in promoters&amp;lt;br&amp;gt;- For whole set of given TF&#039;s binding sites estimate probability of C&amp;amp;gt;T SNP (in CG or in CNG) and of C&amp;amp;gt;T interlineage substitution &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;We have data for functional analysis&#039;&#039;&#039;:&lt;br /&gt;
&lt;br /&gt;
Primary cells: &amp;lt;br&amp;gt;peripheral blood mononuclear cells PBMC (genome-wide BS-seq + CAGE)&amp;lt;br&amp;gt;&lt;br /&gt;
Tissues:&amp;lt;br&amp;gt;frontal cortex (genome-wide MeDIP-seq) - frontal lobe (CAGE)&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;We seek for data&#039;&#039;&#039;:&lt;br /&gt;
DNA methylation with single bp resolution (genome-wide or with coverage of not less when 1% of genome) in primary cells, tissues or cell lines represented in FANTOM5 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&#039;&#039;&#039;Collaboration&#039;&#039;&#039;: &lt;br /&gt;
Piotr (you are invited to add your plans of study on influence of TF on methylation) &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;== TF binding affects DNA methylation == &#039;&#039;&#039; &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Collaborators are very welcome. If you have any ideas how to improve the research, please contact me directly or add your suggestion here. &amp;lt;br&amp;gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=DNA_methylation_and_transcription&amp;diff=1560</id>
		<title>DNA methylation and transcription</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=DNA_methylation_and_transcription&amp;diff=1560"/>
		<updated>2011-03-03T07:21:06Z</updated>

		<summary type="html">&lt;p&gt;Yulia: DNA methylation and transcription&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&#039;&#039;&#039; == DNA methylation affects TF binding and transcription == &#039;&#039;&#039;&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Introduction: It&#039;s commonly accepted that DNA methylation of a promoter repress transcription of this gene in normal tissues. Recently, a class of actively expressed genes having relatively methylated promoters has been discovered. &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Our purposes&#039;&#039;&#039;: &lt;br /&gt;
&lt;br /&gt;
* To explore the idea that DNA methylation affects TFBS, preventing some TF from binding to DNA, and therefore represses transcription.&amp;lt;br&amp;gt;&lt;br /&gt;
* To select TFs most likely sensitive to DNA methylation (first, in human, mb in other spicies later)&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;We plan to do&#039;&#039;&#039;:&lt;br /&gt;
&lt;br /&gt;
1. Functional analysis&amp;lt;br&amp;gt;- Predict TFBS (TFBS clusters?) in promoters&amp;lt;br&amp;gt;- Estimate methylation level of each TFBS (may be, only core positions of TFBS)&amp;lt;br&amp;gt;- Calculate correlation between level of methylation and expression from given promoter for each TFBS&amp;lt;br&amp;gt;- Select lists of TFs with highest and lowest cc&amp;lt;br&amp;gt;2. Evolutionary analysis&amp;lt;br&amp;gt;- Predict TFBS (TFBS clusters?) in promoters&amp;lt;br&amp;gt;- For whole set of given TF&#039;s binding sites estimate probability of C&amp;amp;gt;T SNP (in CG or in CNG) and of C&amp;amp;gt;T interlineage substitution &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;We have data&#039;&#039;&#039;:&lt;br /&gt;
Primary cells: &amp;lt;br&amp;gt;peripheral blood mononuclear cells (genome-wide BS-seq + CAGE)&amp;lt;br&amp;gt;&lt;br /&gt;
Tissues:&amp;lt;br&amp;gt;frontal cortex (genome-wide MeDIP-seq) - frontal lobe (CAGE)&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;We seek for data&#039;&#039;&#039;:&lt;br /&gt;
DNA methyaltion with single bp resolution (genome-wide or with coverage of not less when 1% of genome) in primary cells, tissues or cell lines represented in FANTOM5 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&#039;&#039;&#039;Collaboration&#039;&#039;&#039;: &lt;br /&gt;
Piotr (you are invited to add your plans of study on influence of TF on methylation) &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;== TF binding affects DNA methylation == &#039;&#039;&#039; &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Collaborators are very welcome. If you have any ideas how to improve the research, please contact me directly or add your suggestion here. &amp;lt;br&amp;gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=DNA_methylation_and_transcription&amp;diff=1559</id>
		<title>DNA methylation and transcription</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=DNA_methylation_and_transcription&amp;diff=1559"/>
		<updated>2011-03-03T07:15:57Z</updated>

		<summary type="html">&lt;p&gt;Yulia: DNA methylation and transcription&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&#039;&#039;&#039;DNA methylation affects TF binding and transcription&#039;&#039;&#039;&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
Inroduction: It&#039;s commonly accepted that DNA methylation of a promoter repress transcription of this gene in normal tissues. Recently, a class of actively expressed genes having relatively methylated promoters has been discovered. &amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
Our purposes: &lt;br /&gt;
&lt;br /&gt;
* To explore the idea that DNA methylation affects TFBS, preventing some TF from binding to DNA, and therefore represses transcription. &amp;lt;br&amp;gt;* To select TFs most likely sensitive to DNA methylation (first, in human, mb in other spicies later)&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
We plan to do:&amp;lt;br&amp;gt;1. Functional analysis&amp;lt;br&amp;gt;- Predict TFBS (TFBS clusters?) in promoters&amp;lt;br&amp;gt;- Estimate methylation level of each TFBS (may be, only core positions of TFBS)&amp;lt;br&amp;gt;- Calculate correlation between level of methylation and expression from given promoter for each TFBS&amp;lt;br&amp;gt;- Select lists of TFs with highest and lowest cc&amp;lt;br&amp;gt;2. Evolutionary analysis&amp;lt;br&amp;gt;- Predict TFBS (TFBS clusters?) in promoters&amp;lt;br&amp;gt;- For whole set of given TF&#039;s binding sites estimate probability of C&amp;amp;gt;T SNP (in CG or in CNG) and of C&amp;amp;gt;T interlineage substitution &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
We have data:&amp;lt;br&amp;gt;Primary cells: &amp;lt;br&amp;gt;peripheral blood mononuclear cells (genome-wide BS-seq + CAGE)&amp;lt;br&amp;gt;Tissues:&amp;lt;br&amp;gt;frontal cortex (genome-wide MeDIP-seq) - frontal lobe (CAGE)&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
We seek for data:&amp;lt;br&amp;gt;DNA methyaltion with single bp resolution (genome-wide or with coverage of not less when 1% of genome) in primary cells, tissues or cell lines represented in FANTOM5&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Collaboration: Piotr (you are invited to add your plans of study on influence of TF on methylation)&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;TF binding affects DNA methylation&#039;&#039;&#039; &amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
Collaborators are very welcome. If you have any ideas how to improve the research, please contact me directly or add your suggestion here. &amp;lt;br&amp;gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_papers&amp;diff=1558</id>
		<title>Satellite papers</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_papers&amp;diff=1558"/>
		<updated>2011-03-03T06:55:05Z</updated>

		<summary type="html">&lt;p&gt;Yulia: /* DNA methylation affects TF binding and transcription (Yulia) */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;= Instructions  =&lt;br /&gt;
&lt;br /&gt;
Below you can find the list of satellite paper proposals collected in the February meeting. Please add the following information to each of the proposals &lt;br /&gt;
&lt;br /&gt;
*Check the title &lt;br /&gt;
*provide brief outline of the proposal &lt;br /&gt;
*add/remove your name in case you are interested to work on this satellite paper&lt;br /&gt;
&lt;br /&gt;
Proposal for satellites papers 2/25/2011 Purpose: list up potential satellites; avoid redundancies, make better papers Figure out potential titles to discuss how to negotiate with specific journals. &lt;br /&gt;
&lt;br /&gt;
Add a set of sentences (mini abstract) on the wiki and write an abstract &lt;br /&gt;
&lt;br /&gt;
= Bioinformatics analysis methods  =&lt;br /&gt;
&lt;br /&gt;
== Normalization and clustering issues  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: Tom Freeman&lt;br /&gt;
&lt;br /&gt;
== Modulation of gene expression (Jess Mar)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Expanding transcriptional reg. networks (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Tag clusterin in helicos CAGE (Cesare)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Computational methods for networks comparisons (cesare)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: FBK (C. Furlanello, G: Jurman, ...)&amp;amp;nbsp;&lt;br /&gt;
&lt;br /&gt;
== Tool to make the promoter subsets at will (do not ask us datasets!) (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Delve tag mapping paper (Timo L)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Methods paper on Delve: a probabilistic read mapper. &lt;br /&gt;
*Group members: Timo Lassmann, Carsten Daub&lt;br /&gt;
&lt;br /&gt;
== Classification of CAGE peaks (Timo L)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Deeply sequenced CAGE libraries capture signals on many non-promoter regions. The purpose of this paper is to describe a strategy to separate TSS from non-TSS CAGE peaks (see: [[Media:CAGE_classification.pdf]]). Preliminary work suggest that further sub-classicifation of promoters based on the shape of the CAGE signal is possible (see: [[Media:Brood_october_2010.pdf]]). &lt;br /&gt;
*Group members: Timo Lassmann, Ben Brown, Colin Semple&lt;br /&gt;
&lt;br /&gt;
== Peak finder-noise elimination contest paper (all runners)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Genomics-broad scale analysis  =&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Alternative TSS in cancer relevant to biomarkers (Win Hide)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Impact of alternative promoters on biology of genes (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== How much do we need to sequence? Complexity of the transcriptome (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Revised analysis of zinc finger proteins (Tim Ravasi, David Hume)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Identification of distal regulation elements: role of enhancers in differentiation (Carsten, Boris, Ana P, Jose, YH)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== miRNA promoters (Hideya K, Eivind Al, )  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== CAGE tags on Pigs: Gain and loss of promoters (David Hume) [satellite of the pig genome]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulatory transcription outside canonical promoters (Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Transcription initiation in embryo development (Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Promoters with multiple TSS configuration-multiple ways to use the same promoters (Boris, Kawaji)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Link Fantom 5 to genetic datasets (Peter Heutink; Juha K)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Genome Wide Association Studies (GWAS) have been very succesfull in identifying new risk loci for multifactorial human disease. It has however been very difficult to identify the true biologically relevant variant. GWAS studies in general do not directly test the unknown causal variant but a variant that is in Linkage Disequilibrium with the causal variant. Studies to identify the causal variants are complicated by the observation that most signals from GWAS studies point to non-coding regions of the genome for which the functions are currently unknown. The dataset generated by FANTOM5 now allows to investigate the regions around the association signal for functional elements involved in transcription.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Research method: We have developed a statistical method to delineate the critical region for GWAS loci (Bochdanovits et al. Submitted). We aim to use this method on all publically available GWAS datasets in order to obtain the boundaries of identified GWAS loci. We will then superinpose these genomic region on FANTOM5 data from relevant tissues/celltypes for the disease and identify possible promoters. By using data from the 1000 Genomes project we will investigate if genomic variation exists in the identified promoters. These variants can then be tested for functional effects in cellular reporter assays. &lt;br /&gt;
&lt;br /&gt;
*Group members: Peter Heutink, Juha Kere, Zoltan Bochdanovits and ......please sign up if you are interested.&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
== DNA methylation affects TF binding and transcription (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: It&#039;s commonly accepted that DNA methylation of a promoter repress transcription of this gene in normal tissues. Recently, a class of actively expressed genes having relatively methylated promoters has been discovered. The purpose of this research is to explore the idea that DNA methylation affects CG-rich TFBS, preventing some TF from binding to DNA, and therefore represses transcription.&lt;br /&gt;
&lt;br /&gt;
*Details: [[DNA_methylation_and_transcription]]&lt;br /&gt;
&lt;br /&gt;
*Group members: Yulia Medvedeva&lt;br /&gt;
&lt;br /&gt;
== Comparison of different types/feature of promoters and genome features to study specific differences (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Multiple genomics analysis on multiple datasets (Haru) Extension of the validation?  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Prediction of cell transformation states (Win Hide)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Convergent evolution of retrotransposon promoters (Geoff)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Following the model for the anti-apoptosis gene NAIP (Romanish et al., PLoS Genetics, 2007), we will start by screening the mouse and human genomes for instances where two different retrotransposons occupy the same or similar location in protein-coding genes (e.g. an Alu in human, a B2 in mouse). If this happens frequently enough to be interesting, we will overlay the F5 data onto the &amp;quot;convergent&amp;quot; retrotransposons to see how many are transcribed, what role they may have in regulation (e.g. Lunyak et al., Science, 2007) and if the events are more common for some pathways than others (e.g. in embryogenesis or brain development).&amp;lt;br&amp;gt; &lt;br /&gt;
*Group members: Geoff, Piero&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
== Alternative TSS and alternative splicing (Nicolas)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Chimaeric RNA and 3D structure (if it works) (Nicolas)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Annotation of genes involved in biochemical, metabolic processes and signature for processes-for instance signature for tumors – expression based GO terms (Tom Freeman) (Richard Baldarelli, Jackson and GO groups) (David Hume)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
= Blood group: fill in the holes, more discussion  =&lt;br /&gt;
&lt;br /&gt;
== Granulopoiesis analysis (Andreas Lenn.+Erik Arner)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Eritropoiesis (Peter K)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== HSC (Sugiyama san)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Macrophages (DH)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Subpopulations T cells and monocytes (Michael R)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Brain groups 4 papers Other priority areas in brain: discuss other brain and diseases (YH)  =&lt;br /&gt;
&lt;br /&gt;
== Evolution gene expression in vertebrates Martin + Peter Heutink  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Study the evolution of gene expression combining insights from each of the following: &lt;br /&gt;
**Gene/transcript level changes in expression (and estimating it&#039;s constraint/diversification). &lt;br /&gt;
**TSS/promoter turnover: orthologous genes using non-orthologous promoters, or changes in promoter-preference for one cell type between species. &lt;br /&gt;
**Sequence evolution of core promoters and distant regulatory blocks correlated with changes in gene expression. &lt;br /&gt;
*Focus of the paper on the well matched cells between ((Human, (Macaque?)),(Mouse, Rat),Dog),Chicken) for which we have hCAGE data. (Cell types: Hepatocytes, Aortic smooth muscle cells, mesenchymal stem cells). &lt;br /&gt;
*Group members: Martin Taylor, Peter Heutink, Alison Meynert &lt;br /&gt;
*Details: [[Evolution in gene expression]].&lt;br /&gt;
&lt;br /&gt;
== Transcriptional constrains seq evolution [Martin+Michiel talk]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: [Michiel:] Network analysis across organisms &amp;amp;amp; evolution of regulatory networks, in particular of developmental networks. Are there any subnetworks particularly conserved between organisms? What does this tell us about the functional importance and relevance of specific subnetworks? Do we see any recurring patterns in the network (Uri Alon-type feed-forward loops)? What are the conservation patterns and rates of divergence of transcription factors and specific regulatory relations? Do we see turnover of TFBSs, or do we see conservation of TFBSs in alignments? This can be applied specifically to brain, or more generally to all CAGE samples. TFBS prediction in Neanderthal compared to Homo sapiens would be really cool. &lt;br /&gt;
*Group members: Martin, Michiel, Peter Heutink &lt;br /&gt;
*Martin&#039;s and Michiel&#039;s idea for this paper may overlap or may be complementary to each other; we need to discuss this. This may end up as two satellite papers or one integrated one.&lt;br /&gt;
&lt;br /&gt;
== Tfbs turnover in liver (integrate with ChIP seq) Martin  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Integration of cross-species ChIP-seq data in liver with proximal CAGE tag cluster responses in the same species. Data on liver ChIP-seq for the transcription factors HNF1A and CEBPA in human/mouse/dog/(chicken) Schmidt et al, Science 2010 has been obtained. The questions we can address with this study are: &lt;br /&gt;
**Are conserved binding sites more likely than non-conserved sites to elicit a local, hepatocyte specific ranscriptional response? (Use CEBPA non-expressing cells to generate a background model of proximal transcriptional responses). This could be used to estimate &amp;quot;functional turnover&amp;quot; as opposed to the &amp;quot;binding turnover&amp;quot; as reported by Duncan Odom. &lt;br /&gt;
**Does hepatocyte specific expression (around binding sites) segregate through species lineages with the experimentally defined binding site? &lt;br /&gt;
**If there is apparent turn-over of binding sites, is the pattern of local responsive transcription conserved? &lt;br /&gt;
**Do we see conservation of hepatocyte specific transcriptional responses even in the absence of binding site conservation? &lt;br /&gt;
*Group members: Martin Taylor, Alison Meynert&lt;br /&gt;
&lt;br /&gt;
== Disease paper (brain): human post mortem, … comparison healthy-disease Peter Heutink + Gustincich group  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Rett syndrome and visual cortex Alka  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Genomic architecture in 3 genes involved in Rett syndrome Alka  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Genomic architecture of neurodegenerative disease (Gustincich talk P.H., etc.)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Others  =&lt;br /&gt;
&lt;br /&gt;
== [[Olfactory receptors]]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Promoters of [[Olfactory receptors]] (ORs) are still poorly documented. We have an unpublished promoter list for mouse, and CAGE libraries from human olfactory mucosa will be made. We will identify the promoters of the human ORs and analyse their structure. Many ORs have [[Alternative Promoters|alternative promoters]] and this is a potential example for the promotorome paper. Human-specific OR promoters might be found. There is evidence of expression of the ORs outside the mouse and human olfactory mucosa, and this satellite paper will report this. Experiments to find a ligand and propose a function may be carried out. More information on the page: [[Olfactory receptors]]. &lt;br /&gt;
*Group members: [[User:Plessy|Charles Plessy]], Giovanni Pascarella, Stefano Gustincich and others, but I am too shy to add their name without asking.&lt;br /&gt;
&lt;br /&gt;
== Cell-Cell communicatome (Al forrest)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Drugable cells: drug targets (Al Forrest)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Definition of stem or precursors relationship (Claudio Schneider)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Gene regulation in cells of connective tissues (Vlad, Kim)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Transdifferentiation and network rewiring (Haru; WP6 + others) POTENTIAL main paper for later stage  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Network in cancer (Rama, win’s group)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulatory network in cell lineage tree (Carsten wp5)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Determination of conserved CAGE (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Promoting human uniqueness: human-specific promoters of regulatory lncRNA genes drive cis- and trans-regulation. (LL)  ==&lt;br /&gt;
&lt;br /&gt;
*More information, anticipated Abstract, Definitions, Plan of Work at: [[Regulatory lncRNAs: &#039;promoting&#039; human uniqueness]]&amp;lt;br&amp;gt; &lt;br /&gt;
*Outline: In FANTOM3, we described complex loci -- sense-antisense pairs, bidirectional promoters, and gene chains -- prevalent in mammalian genomes. These complex loci often contain long non-coding RNA (lncRNA) genes not conserved between mouse and human. Now in FANTOM5, our goal is to functionally characterize the specific contribution of non-conserved sequences in human, particularly promoters of lncRNA&amp;amp;nbsp;genes, to gene regulation at complex loci. We will reach this goal by:&amp;amp;nbsp;&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
#identifying all &amp;quot;human-specific&amp;quot; (definition = primate-specific; thus absent in the F5 nonhuman species)&amp;amp;nbsp;promoters in CAGE&amp;amp;nbsp;and CAGEscan data. &amp;lt;br&amp;gt; &lt;br /&gt;
#using Cluster Annotation from the F5 main paper/s to find all lncRNA&amp;amp;nbsp;genes whose promoters are human-specific. &amp;lt;br&amp;gt; &lt;br /&gt;
#determining which lncRNA genes with human-specific promoters are in complex loci, as defined in the first sentence of this Outline.&amp;lt;br&amp;gt; &lt;br /&gt;
#testing each complex locus from #4 for the existence of a unique cis-regulatory expression signature (simple e.g.: all genes in the complex locus are on, all off, or some on and specific others off) that corresponds to a particular, well-defined cell type, tissue type, or steady state. Signatures are defined both by an expression pattern and by an adjacency, overlap, and specific order / orientation of the co-expressed genes neighboring along the genome. &amp;lt;br&amp;gt; &lt;br /&gt;
#determining whether, and how, each complex-locus steady-state-specific expression signature is dependent upon the human-specific promoter of the lncRNA&amp;amp;nbsp;within that signature. (Implementation details are at: [[Regulatory lncRNAs: &#039;promoting&#039; human uniqueness]]&amp;amp;nbsp;)&amp;amp;nbsp; &amp;lt;br&amp;gt; &lt;br /&gt;
#performing, for lncRNAs of exceptional interest from #5, reverse-genetic experiments in cell culture to validate whether the human-specific promoter of the lncRNA&amp;amp;nbsp;really has a regulatory impact that contributes to defining a particular steady state. (Note: we would need the OSC&#039;s direct help with wet-lab validations. Let&#039;s discuss.)&amp;amp;nbsp;&amp;lt;br&amp;gt; &lt;br /&gt;
#defining the unique functional proteome space (e.g. gene ontologies? positive selection? brain genes?&amp;amp;nbsp;etc) cis-regulated by human-specific lncRNA promoters. &amp;lt;br&amp;gt; &lt;br /&gt;
#finally, deriving a multidimensional unified cis- and trans-regulatory network that describes human-specific and lncRNA-mediated gene regulation in specific cellular states. (Definition of such a network is at: [[Regulatory lncRNAs: &#039;promoting&#039; human uniqueness]]&amp;amp;nbsp;)&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Group members: Leonard Lipovich, Yulia Medvedeva (inviting you to join - please confirm), Vlad Bajic (inviting you to join - please confirm), Jess Mar (inviting you to join - please confirm), and I am also too shy to name (or invite) potential others. Please email me or the F5 list, or please just add yourselves to this page, if you would like to join forces on this.&lt;br /&gt;
&lt;br /&gt;
== Using single direction promoter ti eliminate noise (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Specific transcript (Human) regulation and what are nover TF in human (Haru)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Identification of TFBS by de novo methods (Vlad; Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Predicted homotypic clusters and motif prediction (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Identification fo features of primates specific promoters (?; together with LL)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulation specificity of cells and tissues (Vlad’ s group)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Host pathogen infection relationship; influenza virus, Mycobacteria, Salomonella (Arnab)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Searching for viruses, cryptic viruses (Arnab, mamoon, al, nico)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Deorphanizing transcription factors (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Variation in small RNA population and variation in siRNA machinery (Max)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Cellular restriction of terminal ligases in ubiquitin system (Max)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Papers of individual cells time courses  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== [[Extend rat gene models with CAGEscan]]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Rat gene models sometimes lack a proper 5′&amp;amp;nbsp;UTR. CAGEscan data has been produced using the same RNA (10009-101B8) as the reference FANTOM5 Helicos CAGE library CNhs10612. This experimental data can be used to propose an update of the rat gene models. &lt;br /&gt;
*Group members: [[User:Plessy|Charles Plessy]], Albin Sandelin, other people, please list yourself.&lt;br /&gt;
&lt;br /&gt;
== [[Novel metrics for promoter activity profiles]]  ==&lt;br /&gt;
&lt;br /&gt;
== [[Pathway Fingerprinting]]  ==&lt;br /&gt;
&lt;br /&gt;
== Cellular restriction of epigenomic regulation Erik A. + Andreas Lenn.  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
= Issues: negotiation with sample providers  =&lt;br /&gt;
&lt;br /&gt;
== Encouraged to write paper, but larger stronger papers is perhaps better?  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Talk with collaborator before the datasets is published  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
[[Category:Satellite_paper]]&lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_papers&amp;diff=1557</id>
		<title>Satellite papers</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_papers&amp;diff=1557"/>
		<updated>2011-03-03T06:52:32Z</updated>

		<summary type="html">&lt;p&gt;Yulia: /* DNA methylation affects TF binding and transcription (Yulia) */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;= Instructions  =&lt;br /&gt;
&lt;br /&gt;
Below you can find the list of satellite paper proposals collected in the February meeting. Please add the following information to each of the proposals &lt;br /&gt;
&lt;br /&gt;
*Check the title &lt;br /&gt;
*provide brief outline of the proposal &lt;br /&gt;
*add/remove your name in case you are interested to work on this satellite paper&lt;br /&gt;
&lt;br /&gt;
Proposal for satellites papers 2/25/2011 Purpose: list up potential satellites; avoid redundancies, make better papers Figure out potential titles to discuss how to negotiate with specific journals. &lt;br /&gt;
&lt;br /&gt;
Add a set of sentences (mini abstract) on the wiki and write an abstract &lt;br /&gt;
&lt;br /&gt;
= Bioinformatics analysis methods  =&lt;br /&gt;
&lt;br /&gt;
== Normalization and clustering issues  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: Tom Freeman&lt;br /&gt;
&lt;br /&gt;
== Modulation of gene expression (Jess Mar)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Expanding transcriptional reg. networks (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Tag clusterin in helicos CAGE (Cesare)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Computational methods for networks comparisons (cesare)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: FBK (C. Furlanello, G: Jurman, ...)&amp;amp;nbsp;&lt;br /&gt;
&lt;br /&gt;
== Tool to make the promoter subsets at will (do not ask us datasets!) (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Delve tag mapping paper (Timo L)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Methods paper on Delve: a probabilistic read mapper. &lt;br /&gt;
*Group members: Timo Lassmann, Carsten Daub&lt;br /&gt;
&lt;br /&gt;
== Classification of CAGE peaks (Timo L)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Deeply sequenced CAGE libraries capture signals on many non-promoter regions. The purpose of this paper is to describe a strategy to separate TSS from non-TSS CAGE peaks (see: [[Media:CAGE_classification.pdf]]). Preliminary work suggest that further sub-classicifation of promoters based on the shape of the CAGE signal is possible (see: [[Media:Brood_october_2010.pdf]]). &lt;br /&gt;
*Group members: Timo Lassmann, Ben Brown, Colin Semple&lt;br /&gt;
&lt;br /&gt;
== Peak finder-noise elimination contest paper (all runners)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Genomics-broad scale analysis  =&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Alternative TSS in cancer relevant to biomarkers (Win Hide)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Impact of alternative promoters on biology of genes (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== How much do we need to sequence? Complexity of the transcriptome (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Revised analysis of zinc finger proteins (Tim Ravasi, David Hume)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Identification of distal regulation elements: role of enhancers in differentiation (Carsten, Boris, Ana P, Jose, YH)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== miRNA promoters (Hideya K, Eivind Al, )  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== CAGE tags on Pigs: Gain and loss of promoters (David Hume) [satellite of the pig genome]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulatory transcription outside canonical promoters (Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Transcription initiation in embryo development (Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Promoters with multiple TSS configuration-multiple ways to use the same promoters (Boris, Kawaji)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Link Fantom 5 to genetic datasets (Peter Heutink; Juha K)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Genome Wide Association Studies (GWAS) have been very succesfull in identifying new risk loci for multifactorial human disease. It has however been very difficult to identify the true biologically relevant variant. GWAS studies in general do not directly test the unknown causal variant but a variant that is in Linkage Disequilibrium with the causal variant. Studies to identify the causal variants are complicated by the observation that most signals from GWAS studies point to non-coding regions of the genome for which the functions are currently unknown. The dataset generated by FANTOM5 now allows to investigate the regions around the association signal for functional elements involved in transcription.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Research method: We have developed a statistical method to delineate the critical region for GWAS loci (Bochdanovits et al. Submitted). We aim to use this method on all publically available GWAS datasets in order to obtain the boundaries of identified GWAS loci. We will then superinpose these genomic region on FANTOM5 data from relevant tissues/celltypes for the disease and identify possible promoters. By using data from the 1000 Genomes project we will investigate if genomic variation exists in the identified promoters. These variants can then be tested for functional effects in cellular reporter assays. &lt;br /&gt;
&lt;br /&gt;
*Group members: Peter Heutink, Juha Kere, Zoltan Bochdanovits and ......please sign up if you are interested.&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
== DNA methylation affects TF binding and transcription (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: It&#039;s commonly accepted that DNA methylation of a promoter repress transcription of this gene in normal tissues. Recently, a class of actively expressed genes having relatively methylated promoters has been discovered. The purpose of this research is to explore the idea that DNA methylation affects CG-rich TFBS, preventing some TF from binding to DNA, and therefore represses transcription.&lt;br /&gt;
&lt;br /&gt;
*Wiki page: [https://fantom5-collaboration.gsc.riken.jp/wiki/index.php/DNA_methylation_and_transcription]&lt;br /&gt;
&lt;br /&gt;
*Group members: Yulia Medvedeva&lt;br /&gt;
&lt;br /&gt;
== Comparison of different types/feature of promoters and genome features to study specific differences (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Multiple genomics analysis on multiple datasets (Haru) Extension of the validation?  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Prediction of cell transformation states (Win Hide)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Convergent evolution of retrotransposon promoters (Geoff)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Following the model for the anti-apoptosis gene NAIP (Romanish et al., PLoS Genetics, 2007), we will start by screening the mouse and human genomes for instances where two different retrotransposons occupy the same or similar location in protein-coding genes (e.g. an Alu in human, a B2 in mouse). If this happens frequently enough to be interesting, we will overlay the F5 data onto the &amp;quot;convergent&amp;quot; retrotransposons to see how many are transcribed, what role they may have in regulation (e.g. Lunyak et al., Science, 2007) and if the events are more common for some pathways than others (e.g. in embryogenesis or brain development).&amp;lt;br&amp;gt; &lt;br /&gt;
*Group members: Geoff, Piero&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
== Alternative TSS and alternative splicing (Nicolas)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Chimaeric RNA and 3D structure (if it works) (Nicolas)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Annotation of genes involved in biochemical, metabolic processes and signature for processes-for instance signature for tumors – expression based GO terms (Tom Freeman) (Richard Baldarelli, Jackson and GO groups) (David Hume)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
= Blood group: fill in the holes, more discussion  =&lt;br /&gt;
&lt;br /&gt;
== Granulopoiesis analysis (Andreas Lenn.+Erik Arner)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Eritropoiesis (Peter K)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== HSC (Sugiyama san)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Macrophages (DH)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Subpopulations T cells and monocytes (Michael R)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Brain groups 4 papers Other priority areas in brain: discuss other brain and diseases (YH)  =&lt;br /&gt;
&lt;br /&gt;
== Evolution gene expression in vertebrates Martin + Peter Heutink  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Study the evolution of gene expression combining insights from each of the following: &lt;br /&gt;
**Gene/transcript level changes in expression (and estimating it&#039;s constraint/diversification). &lt;br /&gt;
**TSS/promoter turnover: orthologous genes using non-orthologous promoters, or changes in promoter-preference for one cell type between species. &lt;br /&gt;
**Sequence evolution of core promoters and distant regulatory blocks correlated with changes in gene expression. &lt;br /&gt;
*Focus of the paper on the well matched cells between ((Human, (Macaque?)),(Mouse, Rat),Dog),Chicken) for which we have hCAGE data. (Cell types: Hepatocytes, Aortic smooth muscle cells, mesenchymal stem cells). &lt;br /&gt;
*Group members: Martin Taylor, Peter Heutink, Alison Meynert &lt;br /&gt;
*Details: [[Evolution in gene expression]].&lt;br /&gt;
&lt;br /&gt;
== Transcriptional constrains seq evolution [Martin+Michiel talk]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: [Michiel:] Network analysis across organisms &amp;amp;amp; evolution of regulatory networks, in particular of developmental networks. Are there any subnetworks particularly conserved between organisms? What does this tell us about the functional importance and relevance of specific subnetworks? Do we see any recurring patterns in the network (Uri Alon-type feed-forward loops)? What are the conservation patterns and rates of divergence of transcription factors and specific regulatory relations? Do we see turnover of TFBSs, or do we see conservation of TFBSs in alignments? This can be applied specifically to brain, or more generally to all CAGE samples. TFBS prediction in Neanderthal compared to Homo sapiens would be really cool. &lt;br /&gt;
*Group members: Martin, Michiel, Peter Heutink &lt;br /&gt;
*Martin&#039;s and Michiel&#039;s idea for this paper may overlap or may be complementary to each other; we need to discuss this. This may end up as two satellite papers or one integrated one.&lt;br /&gt;
&lt;br /&gt;
== Tfbs turnover in liver (integrate with ChIP seq) Martin  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Integration of cross-species ChIP-seq data in liver with proximal CAGE tag cluster responses in the same species. Data on liver ChIP-seq for the transcription factors HNF1A and CEBPA in human/mouse/dog/(chicken) Schmidt et al, Science 2010 has been obtained. The questions we can address with this study are: &lt;br /&gt;
**Are conserved binding sites more likely than non-conserved sites to elicit a local, hepatocyte specific ranscriptional response? (Use CEBPA non-expressing cells to generate a background model of proximal transcriptional responses). This could be used to estimate &amp;quot;functional turnover&amp;quot; as opposed to the &amp;quot;binding turnover&amp;quot; as reported by Duncan Odom. &lt;br /&gt;
**Does hepatocyte specific expression (around binding sites) segregate through species lineages with the experimentally defined binding site? &lt;br /&gt;
**If there is apparent turn-over of binding sites, is the pattern of local responsive transcription conserved? &lt;br /&gt;
**Do we see conservation of hepatocyte specific transcriptional responses even in the absence of binding site conservation? &lt;br /&gt;
*Group members: Martin Taylor, Alison Meynert&lt;br /&gt;
&lt;br /&gt;
== Disease paper (brain): human post mortem, … comparison healthy-disease Peter Heutink + Gustincich group  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Rett syndrome and visual cortex Alka  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Genomic architecture in 3 genes involved in Rett syndrome Alka  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Genomic architecture of neurodegenerative disease (Gustincich talk P.H., etc.)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Others  =&lt;br /&gt;
&lt;br /&gt;
== [[Olfactory receptors]]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Promoters of [[Olfactory receptors]] (ORs) are still poorly documented. We have an unpublished promoter list for mouse, and CAGE libraries from human olfactory mucosa will be made. We will identify the promoters of the human ORs and analyse their structure. Many ORs have [[Alternative Promoters|alternative promoters]] and this is a potential example for the promotorome paper. Human-specific OR promoters might be found. There is evidence of expression of the ORs outside the mouse and human olfactory mucosa, and this satellite paper will report this. Experiments to find a ligand and propose a function may be carried out. More information on the page: [[Olfactory receptors]]. &lt;br /&gt;
*Group members: [[User:Plessy|Charles Plessy]], Giovanni Pascarella, Stefano Gustincich and others, but I am too shy to add their name without asking.&lt;br /&gt;
&lt;br /&gt;
== Cell-Cell communicatome (Al forrest)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Drugable cells: drug targets (Al Forrest)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Definition of stem or precursors relationship (Claudio Schneider)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Gene regulation in cells of connective tissues (Vlad, Kim)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Transdifferentiation and network rewiring (Haru; WP6 + others) POTENTIAL main paper for later stage  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Network in cancer (Rama, win’s group)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulatory network in cell lineage tree (Carsten wp5)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Determination of conserved CAGE (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Promoting human uniqueness: human-specific promoters of regulatory lncRNA genes drive cis- and trans-regulation. (LL)  ==&lt;br /&gt;
&lt;br /&gt;
*More information, anticipated Abstract, Definitions, Plan of Work at: [[Regulatory lncRNAs: &#039;promoting&#039; human uniqueness]]&amp;lt;br&amp;gt; &lt;br /&gt;
*Outline: In FANTOM3, we described complex loci -- sense-antisense pairs, bidirectional promoters, and gene chains -- prevalent in mammalian genomes. These complex loci often contain long non-coding RNA (lncRNA) genes not conserved between mouse and human. Now in FANTOM5, our goal is to functionally characterize the specific contribution of non-conserved sequences in human, particularly promoters of lncRNA&amp;amp;nbsp;genes, to gene regulation at complex loci. We will reach this goal by:&amp;amp;nbsp;&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
#identifying all &amp;quot;human-specific&amp;quot; (definition = primate-specific; thus absent in the F5 nonhuman species)&amp;amp;nbsp;promoters in CAGE&amp;amp;nbsp;and CAGEscan data. &amp;lt;br&amp;gt; &lt;br /&gt;
#using Cluster Annotation from the F5 main paper/s to find all lncRNA&amp;amp;nbsp;genes whose promoters are human-specific. &amp;lt;br&amp;gt; &lt;br /&gt;
#determining which lncRNA genes with human-specific promoters are in complex loci, as defined in the first sentence of this Outline.&amp;lt;br&amp;gt; &lt;br /&gt;
#testing each complex locus from #4 for the existence of a unique cis-regulatory expression signature (simple e.g.: all genes in the complex locus are on, all off, or some on and specific others off) that corresponds to a particular, well-defined cell type, tissue type, or steady state. Signatures are defined both by an expression pattern and by an adjacency, overlap, and specific order / orientation of the co-expressed genes neighboring along the genome. &amp;lt;br&amp;gt; &lt;br /&gt;
#determining whether, and how, each complex-locus steady-state-specific expression signature is dependent upon the human-specific promoter of the lncRNA&amp;amp;nbsp;within that signature. (Implementation details are at: [[Regulatory lncRNAs: &#039;promoting&#039; human uniqueness]]&amp;amp;nbsp;)&amp;amp;nbsp; &amp;lt;br&amp;gt; &lt;br /&gt;
#performing, for lncRNAs of exceptional interest from #5, reverse-genetic experiments in cell culture to validate whether the human-specific promoter of the lncRNA&amp;amp;nbsp;really has a regulatory impact that contributes to defining a particular steady state. (Note: we would need the OSC&#039;s direct help with wet-lab validations. Let&#039;s discuss.)&amp;amp;nbsp;&amp;lt;br&amp;gt; &lt;br /&gt;
#defining the unique functional proteome space (e.g. gene ontologies? positive selection? brain genes?&amp;amp;nbsp;etc) cis-regulated by human-specific lncRNA promoters. &amp;lt;br&amp;gt; &lt;br /&gt;
#finally, deriving a multidimensional unified cis- and trans-regulatory network that describes human-specific and lncRNA-mediated gene regulation in specific cellular states. (Definition of such a network is at: [[Regulatory lncRNAs: &#039;promoting&#039; human uniqueness]]&amp;amp;nbsp;)&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Group members: Leonard Lipovich, Yulia Medvedeva (inviting you to join - please confirm), Vlad Bajic (inviting you to join - please confirm), Jess Mar (inviting you to join - please confirm), and I am also too shy to name (or invite) potential others. Please email me or the F5 list, or please just add yourselves to this page, if you would like to join forces on this.&lt;br /&gt;
&lt;br /&gt;
== Using single direction promoter ti eliminate noise (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Specific transcript (Human) regulation and what are nover TF in human (Haru)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Identification of TFBS by de novo methods (Vlad; Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Predicted homotypic clusters and motif prediction (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Identification fo features of primates specific promoters (?; together with LL)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulation specificity of cells and tissues (Vlad’ s group)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Host pathogen infection relationship; influenza virus, Mycobacteria, Salomonella (Arnab)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Searching for viruses, cryptic viruses (Arnab, mamoon, al, nico)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Deorphanizing transcription factors (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Variation in small RNA population and variation in siRNA machinery (Max)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Cellular restriction of terminal ligases in ubiquitin system (Max)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Papers of individual cells time courses  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== [[Extend rat gene models with CAGEscan]]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Rat gene models sometimes lack a proper 5′&amp;amp;nbsp;UTR. CAGEscan data has been produced using the same RNA (10009-101B8) as the reference FANTOM5 Helicos CAGE library CNhs10612. This experimental data can be used to propose an update of the rat gene models. &lt;br /&gt;
*Group members: [[User:Plessy|Charles Plessy]], Albin Sandelin, other people, please list yourself.&lt;br /&gt;
&lt;br /&gt;
== [[Novel metrics for promoter activity profiles]]  ==&lt;br /&gt;
&lt;br /&gt;
== [[Pathway Fingerprinting]]  ==&lt;br /&gt;
&lt;br /&gt;
== Cellular restriction of epigenomic regulation Erik A. + Andreas Lenn.  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
= Issues: negotiation with sample providers  =&lt;br /&gt;
&lt;br /&gt;
== Encouraged to write paper, but larger stronger papers is perhaps better?  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Talk with collaborator before the datasets is published  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
[[Category:Satellite_paper]]&lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_papers&amp;diff=1556</id>
		<title>Satellite papers</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_papers&amp;diff=1556"/>
		<updated>2011-03-03T06:50:59Z</updated>

		<summary type="html">&lt;p&gt;Yulia: /* DNA methylation affects TF binding and transcription (Yulia) */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;= Instructions  =&lt;br /&gt;
&lt;br /&gt;
Below you can find the list of satellite paper proposals collected in the February meeting. Please add the following information to each of the proposals &lt;br /&gt;
&lt;br /&gt;
*Check the title &lt;br /&gt;
*provide brief outline of the proposal &lt;br /&gt;
*add/remove your name in case you are interested to work on this satellite paper&lt;br /&gt;
&lt;br /&gt;
Proposal for satellites papers 2/25/2011 Purpose: list up potential satellites; avoid redundancies, make better papers Figure out potential titles to discuss how to negotiate with specific journals. &lt;br /&gt;
&lt;br /&gt;
Add a set of sentences (mini abstract) on the wiki and write an abstract &lt;br /&gt;
&lt;br /&gt;
= Bioinformatics analysis methods  =&lt;br /&gt;
&lt;br /&gt;
== Normalization and clustering issues  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: Tom Freeman&lt;br /&gt;
&lt;br /&gt;
== Modulation of gene expression (Jess Mar)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Expanding transcriptional reg. networks (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Tag clusterin in helicos CAGE (Cesare)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Computational methods for networks comparisons (cesare)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: FBK (C. Furlanello, G: Jurman, ...)&amp;amp;nbsp;&lt;br /&gt;
&lt;br /&gt;
== Tool to make the promoter subsets at will (do not ask us datasets!) (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Delve tag mapping paper (Timo L)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Methods paper on Delve: a probabilistic read mapper. &lt;br /&gt;
*Group members: Timo Lassmann, Carsten Daub&lt;br /&gt;
&lt;br /&gt;
== Classification of CAGE peaks (Timo L)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Deeply sequenced CAGE libraries capture signals on many non-promoter regions. The purpose of this paper is to describe a strategy to separate TSS from non-TSS CAGE peaks (see: [[Media:CAGE_classification.pdf]]). Preliminary work suggest that further sub-classicifation of promoters based on the shape of the CAGE signal is possible (see: [[Media:Brood_october_2010.pdf]]). &lt;br /&gt;
*Group members: Timo Lassmann, Ben Brown, Colin Semple&lt;br /&gt;
&lt;br /&gt;
== Peak finder-noise elimination contest paper (all runners)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Genomics-broad scale analysis  =&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Alternative TSS in cancer relevant to biomarkers (Win Hide)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Impact of alternative promoters on biology of genes (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== How much do we need to sequence? Complexity of the transcriptome (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Revised analysis of zinc finger proteins (Tim Ravasi, David Hume)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Identification of distal regulation elements: role of enhancers in differentiation (Carsten, Boris, Ana P, Jose, YH)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== miRNA promoters (Hideya K, Eivind Al, )  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== CAGE tags on Pigs: Gain and loss of promoters (David Hume) [satellite of the pig genome]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulatory transcription outside canonical promoters (Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Transcription initiation in embryo development (Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Promoters with multiple TSS configuration-multiple ways to use the same promoters (Boris, Kawaji)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Link Fantom 5 to genetic datasets (Peter Heutink; Juha K)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Genome Wide Association Studies (GWAS) have been very succesfull in identifying new risk loci for multifactorial human disease. It has however been very difficult to identify the true biologically relevant variant. GWAS studies in general do not directly test the unknown causal variant but a variant that is in Linkage Disequilibrium with the causal variant. Studies to identify the causal variants are complicated by the observation that most signals from GWAS studies point to non-coding regions of the genome for which the functions are currently unknown. The dataset generated by FANTOM5 now allows to investigate the regions around the association signal for functional elements involved in transcription.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Research method: We have developed a statistical method to delineate the critical region for GWAS loci (Bochdanovits et al. Submitted). We aim to use this method on all publically available GWAS datasets in order to obtain the boundaries of identified GWAS loci. We will then superinpose these genomic region on FANTOM5 data from relevant tissues/celltypes for the disease and identify possible promoters. By using data from the 1000 Genomes project we will investigate if genomic variation exists in the identified promoters. These variants can then be tested for functional effects in cellular reporter assays. &lt;br /&gt;
&lt;br /&gt;
*Group members: Peter Heutink, Juha Kere, Zoltan Bochdanovits and ......please sign up if you are interested.&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
== DNA methylation affects TF binding and transcription (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: It&#039;s commonly accepted that DNA methylation of a promoter repress transcription of this gene in normal tissues. Recently, a class of actively expressed genes having relatively methylated promoters has been discovered. The purpose of this research is to explore the idea that DNA methylation affects CG-rich TFBS, preventing some TF from binding to DNA, and therefore represses transcription.&lt;br /&gt;
&lt;br /&gt;
*Group members: Yulia Medvedeva&lt;br /&gt;
&lt;br /&gt;
== Comparison of different types/feature of promoters and genome features to study specific differences (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Multiple genomics analysis on multiple datasets (Haru) Extension of the validation?  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Prediction of cell transformation states (Win Hide)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Convergent evolution of retrotransposon promoters (Geoff)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Following the model for the anti-apoptosis gene NAIP (Romanish et al., PLoS Genetics, 2007), we will start by screening the mouse and human genomes for instances where two different retrotransposons occupy the same or similar location in protein-coding genes (e.g. an Alu in human, a B2 in mouse). If this happens frequently enough to be interesting, we will overlay the F5 data onto the &amp;quot;convergent&amp;quot; retrotransposons to see how many are transcribed, what role they may have in regulation (e.g. Lunyak et al., Science, 2007) and if the events are more common for some pathways than others (e.g. in embryogenesis or brain development).&amp;lt;br&amp;gt; &lt;br /&gt;
*Group members: Geoff, Piero&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
== Alternative TSS and alternative splicing (Nicolas)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Chimaeric RNA and 3D structure (if it works) (Nicolas)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Annotation of genes involved in biochemical, metabolic processes and signature for processes-for instance signature for tumors – expression based GO terms (Tom Freeman) (Richard Baldarelli, Jackson and GO groups) (David Hume)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
= Blood group: fill in the holes, more discussion  =&lt;br /&gt;
&lt;br /&gt;
== Granulopoiesis analysis (Andreas Lenn.+Erik Arner)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Eritropoiesis (Peter K)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== HSC (Sugiyama san)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Macrophages (DH)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Subpopulations T cells and monocytes (Michael R)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Brain groups 4 papers Other priority areas in brain: discuss other brain and diseases (YH)  =&lt;br /&gt;
&lt;br /&gt;
== Evolution gene expression in vertebrates Martin + Peter Heutink  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Study the evolution of gene expression combining insights from each of the following: &lt;br /&gt;
**Gene/transcript level changes in expression (and estimating it&#039;s constraint/diversification). &lt;br /&gt;
**TSS/promoter turnover: orthologous genes using non-orthologous promoters, or changes in promoter-preference for one cell type between species. &lt;br /&gt;
**Sequence evolution of core promoters and distant regulatory blocks correlated with changes in gene expression. &lt;br /&gt;
*Focus of the paper on the well matched cells between ((Human, (Macaque?)),(Mouse, Rat),Dog),Chicken) for which we have hCAGE data. (Cell types: Hepatocytes, Aortic smooth muscle cells, mesenchymal stem cells). &lt;br /&gt;
*Group members: Martin Taylor, Peter Heutink, Alison Meynert &lt;br /&gt;
*Details: [[Evolution in gene expression]].&lt;br /&gt;
&lt;br /&gt;
== Transcriptional constrains seq evolution [Martin+Michiel talk]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: [Michiel:] Network analysis across organisms &amp;amp;amp; evolution of regulatory networks, in particular of developmental networks. Are there any subnetworks particularly conserved between organisms? What does this tell us about the functional importance and relevance of specific subnetworks? Do we see any recurring patterns in the network (Uri Alon-type feed-forward loops)? What are the conservation patterns and rates of divergence of transcription factors and specific regulatory relations? Do we see turnover of TFBSs, or do we see conservation of TFBSs in alignments? This can be applied specifically to brain, or more generally to all CAGE samples. TFBS prediction in Neanderthal compared to Homo sapiens would be really cool. &lt;br /&gt;
*Group members: Martin, Michiel, Peter Heutink &lt;br /&gt;
*Martin&#039;s and Michiel&#039;s idea for this paper may overlap or may be complementary to each other; we need to discuss this. This may end up as two satellite papers or one integrated one.&lt;br /&gt;
&lt;br /&gt;
== Tfbs turnover in liver (integrate with ChIP seq) Martin  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Integration of cross-species ChIP-seq data in liver with proximal CAGE tag cluster responses in the same species. Data on liver ChIP-seq for the transcription factors HNF1A and CEBPA in human/mouse/dog/(chicken) Schmidt et al, Science 2010 has been obtained. The questions we can address with this study are: &lt;br /&gt;
**Are conserved binding sites more likely than non-conserved sites to elicit a local, hepatocyte specific ranscriptional response? (Use CEBPA non-expressing cells to generate a background model of proximal transcriptional responses). This could be used to estimate &amp;quot;functional turnover&amp;quot; as opposed to the &amp;quot;binding turnover&amp;quot; as reported by Duncan Odom. &lt;br /&gt;
**Does hepatocyte specific expression (around binding sites) segregate through species lineages with the experimentally defined binding site? &lt;br /&gt;
**If there is apparent turn-over of binding sites, is the pattern of local responsive transcription conserved? &lt;br /&gt;
**Do we see conservation of hepatocyte specific transcriptional responses even in the absence of binding site conservation? &lt;br /&gt;
*Group members: Martin Taylor, Alison Meynert&lt;br /&gt;
&lt;br /&gt;
== Disease paper (brain): human post mortem, … comparison healthy-disease Peter Heutink + Gustincich group  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Rett syndrome and visual cortex Alka  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Genomic architecture in 3 genes involved in Rett syndrome Alka  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Genomic architecture of neurodegenerative disease (Gustincich talk P.H., etc.)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Others  =&lt;br /&gt;
&lt;br /&gt;
== [[Olfactory receptors]]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Promoters of [[Olfactory receptors]] (ORs) are still poorly documented. We have an unpublished promoter list for mouse, and CAGE libraries from human olfactory mucosa will be made. We will identify the promoters of the human ORs and analyse their structure. Many ORs have [[Alternative Promoters|alternative promoters]] and this is a potential example for the promotorome paper. Human-specific OR promoters might be found. There is evidence of expression of the ORs outside the mouse and human olfactory mucosa, and this satellite paper will report this. Experiments to find a ligand and propose a function may be carried out. More information on the page: [[Olfactory receptors]]. &lt;br /&gt;
*Group members: [[User:Plessy|Charles Plessy]], Giovanni Pascarella, Stefano Gustincich and others, but I am too shy to add their name without asking.&lt;br /&gt;
&lt;br /&gt;
== Cell-Cell communicatome (Al forrest)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Drugable cells: drug targets (Al Forrest)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Definition of stem or precursors relationship (Claudio Schneider)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Gene regulation in cells of connective tissues (Vlad, Kim)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Transdifferentiation and network rewiring (Haru; WP6 + others) POTENTIAL main paper for later stage  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Network in cancer (Rama, win’s group)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulatory network in cell lineage tree (Carsten wp5)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Determination of conserved CAGE (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Promoting human uniqueness: human-specific promoters of regulatory lncRNA genes drive cis- and trans-regulation. (LL)  ==&lt;br /&gt;
&lt;br /&gt;
*More information, anticipated Abstract, Definitions, Plan of Work at: [[Regulatory lncRNAs: &#039;promoting&#039; human uniqueness]]&amp;lt;br&amp;gt; &lt;br /&gt;
*Outline: In FANTOM3, we described complex loci -- sense-antisense pairs, bidirectional promoters, and gene chains -- prevalent in mammalian genomes. These complex loci often contain long non-coding RNA (lncRNA) genes not conserved between mouse and human. Now in FANTOM5, our goal is to functionally characterize the specific contribution of non-conserved sequences in human, particularly promoters of lncRNA&amp;amp;nbsp;genes, to gene regulation at complex loci. We will reach this goal by:&amp;amp;nbsp;&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
#identifying all &amp;quot;human-specific&amp;quot; (definition = primate-specific; thus absent in the F5 nonhuman species)&amp;amp;nbsp;promoters in CAGE&amp;amp;nbsp;and CAGEscan data. &amp;lt;br&amp;gt; &lt;br /&gt;
#using Cluster Annotation from the F5 main paper/s to find all lncRNA&amp;amp;nbsp;genes whose promoters are human-specific. &amp;lt;br&amp;gt; &lt;br /&gt;
#determining which lncRNA genes with human-specific promoters are in complex loci, as defined in the first sentence of this Outline.&amp;lt;br&amp;gt; &lt;br /&gt;
#testing each complex locus from #4 for the existence of a unique cis-regulatory expression signature (simple e.g.: all genes in the complex locus are on, all off, or some on and specific others off) that corresponds to a particular, well-defined cell type, tissue type, or steady state. Signatures are defined both by an expression pattern and by an adjacency, overlap, and specific order / orientation of the co-expressed genes neighboring along the genome. &amp;lt;br&amp;gt; &lt;br /&gt;
#determining whether, and how, each complex-locus steady-state-specific expression signature is dependent upon the human-specific promoter of the lncRNA&amp;amp;nbsp;within that signature. (Implementation details are at: [[Regulatory lncRNAs: &#039;promoting&#039; human uniqueness]]&amp;amp;nbsp;)&amp;amp;nbsp; &amp;lt;br&amp;gt; &lt;br /&gt;
#performing, for lncRNAs of exceptional interest from #5, reverse-genetic experiments in cell culture to validate whether the human-specific promoter of the lncRNA&amp;amp;nbsp;really has a regulatory impact that contributes to defining a particular steady state. (Note: we would need the OSC&#039;s direct help with wet-lab validations. Let&#039;s discuss.)&amp;amp;nbsp;&amp;lt;br&amp;gt; &lt;br /&gt;
#defining the unique functional proteome space (e.g. gene ontologies? positive selection? brain genes?&amp;amp;nbsp;etc) cis-regulated by human-specific lncRNA promoters. &amp;lt;br&amp;gt; &lt;br /&gt;
#finally, deriving a multidimensional unified cis- and trans-regulatory network that describes human-specific and lncRNA-mediated gene regulation in specific cellular states. (Definition of such a network is at: [[Regulatory lncRNAs: &#039;promoting&#039; human uniqueness]]&amp;amp;nbsp;)&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Group members: Leonard Lipovich, Yulia Medvedeva (inviting you to join - please confirm), Vlad Bajic (inviting you to join - please confirm), Jess Mar (inviting you to join - please confirm), and I am also too shy to name (or invite) potential others. Please email me or the F5 list, or please just add yourselves to this page, if you would like to join forces on this.&lt;br /&gt;
&lt;br /&gt;
== Using single direction promoter ti eliminate noise (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Specific transcript (Human) regulation and what are nover TF in human (Haru)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Identification of TFBS by de novo methods (Vlad; Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Predicted homotypic clusters and motif prediction (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Identification fo features of primates specific promoters (?; together with LL)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulation specificity of cells and tissues (Vlad’ s group)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Host pathogen infection relationship; influenza virus, Mycobacteria, Salomonella (Arnab)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Searching for viruses, cryptic viruses (Arnab, mamoon, al, nico)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Deorphanizing transcription factors (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Variation in small RNA population and variation in siRNA machinery (Max)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Cellular restriction of terminal ligases in ubiquitin system (Max)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Papers of individual cells time courses  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== [[Extend rat gene models with CAGEscan]]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Rat gene models sometimes lack a proper 5′&amp;amp;nbsp;UTR. CAGEscan data has been produced using the same RNA (10009-101B8) as the reference FANTOM5 Helicos CAGE library CNhs10612. This experimental data can be used to propose an update of the rat gene models. &lt;br /&gt;
*Group members: [[User:Plessy|Charles Plessy]], Albin Sandelin, other people, please list yourself.&lt;br /&gt;
&lt;br /&gt;
== [[Novel metrics for promoter activity profiles]]  ==&lt;br /&gt;
&lt;br /&gt;
== [[Pathway Fingerprinting]]  ==&lt;br /&gt;
&lt;br /&gt;
== Cellular restriction of epigenomic regulation Erik A. + Andreas Lenn.  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
= Issues: negotiation with sample providers  =&lt;br /&gt;
&lt;br /&gt;
== Encouraged to write paper, but larger stronger papers is perhaps better?  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Talk with collaborator before the datasets is published  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
[[Category:Satellite_paper]]&lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_papers&amp;diff=1555</id>
		<title>Satellite papers</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_papers&amp;diff=1555"/>
		<updated>2011-03-03T06:46:20Z</updated>

		<summary type="html">&lt;p&gt;Yulia: /* DNA methylation affects TF binding and expression (Yulia) */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;= Instructions  =&lt;br /&gt;
&lt;br /&gt;
Below you can find the list of satellite paper proposals collected in the February meeting. Please add the following information to each of the proposals &lt;br /&gt;
&lt;br /&gt;
*Check the title &lt;br /&gt;
*provide brief outline of the proposal &lt;br /&gt;
*add/remove your name in case you are interested to work on this satellite paper&lt;br /&gt;
&lt;br /&gt;
Proposal for satellites papers 2/25/2011 Purpose: list up potential satellites; avoid redundancies, make better papers Figure out potential titles to discuss how to negotiate with specific journals. &lt;br /&gt;
&lt;br /&gt;
Add a set of sentences (mini abstract) on the wiki and write an abstract &lt;br /&gt;
&lt;br /&gt;
= Bioinformatics analysis methods  =&lt;br /&gt;
&lt;br /&gt;
== Normalization and clustering issues  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: Tom Freeman&lt;br /&gt;
&lt;br /&gt;
== Modulation of gene expression (Jess Mar)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Expanding transcriptional reg. networks (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Tag clusterin in helicos CAGE (Cesare)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Computational methods for networks comparisons (cesare)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: FBK (C. Furlanello, G: Jurman, ...)&amp;amp;nbsp;&lt;br /&gt;
&lt;br /&gt;
== Tool to make the promoter subsets at will (do not ask us datasets!) (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Delve tag mapping paper (Timo L)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Methods paper on Delve: a probabilistic read mapper. &lt;br /&gt;
*Group members: Timo Lassmann, Carsten Daub&lt;br /&gt;
&lt;br /&gt;
== Classification of CAGE peaks (Timo L)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Deeply sequenced CAGE libraries capture signals on many non-promoter regions. The purpose of this paper is to describe a strategy to separate TSS from non-TSS CAGE peaks (see: [[Media:CAGE_classification.pdf]]). Preliminary work suggest that further sub-classicifation of promoters based on the shape of the CAGE signal is possible (see: [[Media:Brood_october_2010.pdf]]). &lt;br /&gt;
*Group members: Timo Lassmann, Ben Brown, Colin Semple&lt;br /&gt;
&lt;br /&gt;
== Peak finder-noise elimination contest paper (all runners)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Genomics-broad scale analysis  =&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Alternative TSS in cancer relevant to biomarkers (Win Hide)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Impact of alternative promoters on biology of genes (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== How much do we need to sequence? Complexity of the transcriptome (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Revised analysis of zinc finger proteins (Tim Ravasi, David Hume)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Identification of distal regulation elements: role of enhancers in differentiation (Carsten, Boris, Ana P, Jose, YH)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== miRNA promoters (Hideya K, Eivind Al, )  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== CAGE tags on Pigs: Gain and loss of promoters (David Hume) [satellite of the pig genome]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulatory transcription outside canonical promoters (Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Transcription initiation in embryo development (Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Promoters with multiple TSS configuration-multiple ways to use the same promoters (Boris, Kawaji)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Link Fantom 5 to genetic datasets (Peter Heutink; Juha K)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Genome Wide Association Studies (GWAS) have been very succesfull in identifying new risk loci for multifactorial human disease. It has however been very difficult to identify the true biologically relevant variant. GWAS studies in general do not directly test the unknown causal variant but a variant that is in Linkage Disequilibrium with the causal variant. Studies to identify the causal variants are complicated by the observation that most signals from GWAS studies point to non-coding regions of the genome for which the functions are currently unknown. The dataset generated by FANTOM5 now allows to investigate the regions around the association signal for functional elements involved in transcription.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Research method: We have developed a statistical method to delineate the critical region for GWAS loci (Bochdanovits et al. Submitted). We aim to use this method on all publically available GWAS datasets in order to obtain the boundaries of identified GWAS loci. We will then superinpose these genomic region on FANTOM5 data from relevant tissues/celltypes for the disease and identify possible promoters. By using data from the 1000 Genomes project we will investigate if genomic variation exists in the identified promoters. These variants can then be tested for functional effects in cellular reporter assays. &lt;br /&gt;
&lt;br /&gt;
*Group members: Peter Heutink, Juha Kere, Zoltan Bochdanovits and ......please sign up if you are interested.&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
== DNA methylation affects TF binding and expression (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: It&#039;s commonly accepted that DNA methylation of a promoter repress transcription of this gene in normal tissues. Recently, a class of actively expressed genes having relatively methylated promoters has been discovered. The purpose of this research is to explore the idea that DNA methylation affects CG-rich TFBS, preventing some TF from binding to DNA, and therefore represses transcription.&lt;br /&gt;
&lt;br /&gt;
*Group members: Yulia Medvedeva&lt;br /&gt;
&lt;br /&gt;
== Comparison of different types/feature of promoters and genome features to study specific differences (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Multiple genomics analysis on multiple datasets (Haru) Extension of the validation?  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Prediction of cell transformation states (Win Hide)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Convergent evolution of retrotransposon promoters (Geoff)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Following the model for the anti-apoptosis gene NAIP (Romanish et al., PLoS Genetics, 2007), we will start by screening the mouse and human genomes for instances where two different retrotransposons occupy the same or similar location in protein-coding genes (e.g. an Alu in human, a B2 in mouse). If this happens frequently enough to be interesting, we will overlay the F5 data onto the &amp;quot;convergent&amp;quot; retrotransposons to see how many are transcribed, what role they may have in regulation (e.g. Lunyak et al., Science, 2007) and if the events are more common for some pathways than others (e.g. in embryogenesis or brain development).&amp;lt;br&amp;gt; &lt;br /&gt;
*Group members: Geoff, Piero&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
== Alternative TSS and alternative splicing (Nicolas)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Chimaeric RNA and 3D structure (if it works) (Nicolas)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Annotation of genes involved in biochemical, metabolic processes and signature for processes-for instance signature for tumors – expression based GO terms (Tom Freeman) (Richard Baldarelli, Jackson and GO groups) (David Hume)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
= Blood group: fill in the holes, more discussion  =&lt;br /&gt;
&lt;br /&gt;
== Granulopoiesis analysis (Andreas Lenn.+Erik Arner)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Eritropoiesis (Peter K)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== HSC (Sugiyama san)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Macrophages (DH)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Subpopulations T cells and monocytes (Michael R)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Brain groups 4 papers Other priority areas in brain: discuss other brain and diseases (YH)  =&lt;br /&gt;
&lt;br /&gt;
== Evolution gene expression in vertebrates Martin + Peter Heutink  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Study the evolution of gene expression combining insights from each of the following: &lt;br /&gt;
**Gene/transcript level changes in expression (and estimating it&#039;s constraint/diversification). &lt;br /&gt;
**TSS/promoter turnover: orthologous genes using non-orthologous promoters, or changes in promoter-preference for one cell type between species. &lt;br /&gt;
**Sequence evolution of core promoters and distant regulatory blocks correlated with changes in gene expression. &lt;br /&gt;
*Focus of the paper on the well matched cells between ((Human, (Macaque?)),(Mouse, Rat),Dog),Chicken) for which we have hCAGE data. (Cell types: Hepatocytes, Aortic smooth muscle cells, mesenchymal stem cells). &lt;br /&gt;
*Group members: Martin Taylor, Peter Heutink, Alison Meynert &lt;br /&gt;
*Details: [[Evolution in gene expression]].&lt;br /&gt;
&lt;br /&gt;
== Transcriptional constrains seq evolution [Martin+Michiel talk]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: [Michiel:] Network analysis across organisms &amp;amp;amp; evolution of regulatory networks, in particular of developmental networks. Are there any subnetworks particularly conserved between organisms? What does this tell us about the functional importance and relevance of specific subnetworks? Do we see any recurring patterns in the network (Uri Alon-type feed-forward loops)? What are the conservation patterns and rates of divergence of transcription factors and specific regulatory relations? Do we see turnover of TFBSs, or do we see conservation of TFBSs in alignments? This can be applied specifically to brain, or more generally to all CAGE samples. TFBS prediction in Neanderthal compared to Homo sapiens would be really cool. &lt;br /&gt;
*Group members: Martin, Michiel, Peter Heutink &lt;br /&gt;
*Martin&#039;s and Michiel&#039;s idea for this paper may overlap or may be complementary to each other; we need to discuss this. This may end up as two satellite papers or one integrated one.&lt;br /&gt;
&lt;br /&gt;
== Tfbs turnover in liver (integrate with ChIP seq) Martin  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Integration of cross-species ChIP-seq data in liver with proximal CAGE tag cluster responses in the same species. Data on liver ChIP-seq for the transcription factors HNF1A and CEBPA in human/mouse/dog/(chicken) Schmidt et al, Science 2010 has been obtained. The questions we can address with this study are: &lt;br /&gt;
**Are conserved binding sites more likely than non-conserved sites to elicit a local, hepatocyte specific ranscriptional response? (Use CEBPA non-expressing cells to generate a background model of proximal transcriptional responses). This could be used to estimate &amp;quot;functional turnover&amp;quot; as opposed to the &amp;quot;binding turnover&amp;quot; as reported by Duncan Odom. &lt;br /&gt;
**Does hepatocyte specific expression (around binding sites) segregate through species lineages with the experimentally defined binding site? &lt;br /&gt;
**If there is apparent turn-over of binding sites, is the pattern of local responsive transcription conserved? &lt;br /&gt;
**Do we see conservation of hepatocyte specific transcriptional responses even in the absence of binding site conservation? &lt;br /&gt;
*Group members: Martin Taylor, Alison Meynert&lt;br /&gt;
&lt;br /&gt;
== Disease paper (brain): human post mortem, … comparison healthy-disease Peter Heutink + Gustincich group  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Rett syndrome and visual cortex Alka  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Genomic architecture in 3 genes involved in Rett syndrome Alka  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Genomic architecture of neurodegenerative disease (Gustincich talk P.H., etc.)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Others  =&lt;br /&gt;
&lt;br /&gt;
== [[Olfactory receptors]]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Promoters of [[Olfactory receptors]] (ORs) are still poorly documented. We have an unpublished promoter list for mouse, and CAGE libraries from human olfactory mucosa will be made. We will identify the promoters of the human ORs and analyse their structure. Many ORs have [[Alternative Promoters|alternative promoters]] and this is a potential example for the promotorome paper. Human-specific OR promoters might be found. There is evidence of expression of the ORs outside the mouse and human olfactory mucosa, and this satellite paper will report this. Experiments to find a ligand and propose a function may be carried out. More information on the page: [[Olfactory receptors]]. &lt;br /&gt;
*Group members: [[User:Plessy|Charles Plessy]], Giovanni Pascarella, Stefano Gustincich and others, but I am too shy to add their name without asking.&lt;br /&gt;
&lt;br /&gt;
== Cell-Cell communicatome (Al forrest)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Drugable cells: drug targets (Al Forrest)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Definition of stem or precursors relationship (Claudio Schneider)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Gene regulation in cells of connective tissues (Vlad, Kim)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Transdifferentiation and network rewiring (Haru; WP6 + others) POTENTIAL main paper for later stage  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Network in cancer (Rama, win’s group)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulatory network in cell lineage tree (Carsten wp5)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Determination of conserved CAGE (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Promoting human uniqueness: human-specific promoters of regulatory lncRNA genes drive cis- and trans-regulation. (LL)  ==&lt;br /&gt;
&lt;br /&gt;
*More information, anticipated Abstract, Definitions, Plan of Work at: [[Regulatory lncRNAs: &#039;promoting&#039; human uniqueness]]&amp;lt;br&amp;gt; &lt;br /&gt;
*Outline: In FANTOM3, we described complex loci -- sense-antisense pairs, bidirectional promoters, and gene chains -- prevalent in mammalian genomes. These complex loci often contain long non-coding RNA (lncRNA) genes not conserved between mouse and human. Now in FANTOM5, our goal is to functionally characterize the specific contribution of non-conserved sequences in human, particularly promoters of lncRNA&amp;amp;nbsp;genes, to gene regulation at complex loci. We will reach this goal by:&amp;amp;nbsp;&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
#identifying all &amp;quot;human-specific&amp;quot; (definition = primate-specific; thus absent in the F5 nonhuman species)&amp;amp;nbsp;promoters in CAGE&amp;amp;nbsp;and CAGEscan data. &amp;lt;br&amp;gt; &lt;br /&gt;
#using Cluster Annotation from the F5 main paper/s to find all lncRNA&amp;amp;nbsp;genes whose promoters are human-specific. &amp;lt;br&amp;gt; &lt;br /&gt;
#determining which lncRNA genes with human-specific promoters are in complex loci, as defined in the first sentence of this Outline.&amp;lt;br&amp;gt; &lt;br /&gt;
#testing each complex locus from #4 for the existence of a unique cis-regulatory expression signature (simple e.g.: all genes in the complex locus are on, all off, or some on and specific others off) that corresponds to a particular, well-defined cell type, tissue type, or steady state. Signatures are defined both by an expression pattern and by an adjacency, overlap, and specific order / orientation of the co-expressed genes neighboring along the genome. &amp;lt;br&amp;gt; &lt;br /&gt;
#determining whether, and how, each complex-locus steady-state-specific expression signature is dependent upon the human-specific promoter of the lncRNA&amp;amp;nbsp;within that signature. (Implementation details are at: [[Regulatory lncRNAs: &#039;promoting&#039; human uniqueness]]&amp;amp;nbsp;)&amp;amp;nbsp; &amp;lt;br&amp;gt; &lt;br /&gt;
#performing, for lncRNAs of exceptional interest from #5, reverse-genetic experiments in cell culture to validate whether the human-specific promoter of the lncRNA&amp;amp;nbsp;really has a regulatory impact that contributes to defining a particular steady state. (Note: we would need the OSC&#039;s direct help with wet-lab validations. Let&#039;s discuss.)&amp;amp;nbsp;&amp;lt;br&amp;gt; &lt;br /&gt;
#defining the unique functional proteome space (e.g. gene ontologies? positive selection? brain genes?&amp;amp;nbsp;etc) cis-regulated by human-specific lncRNA promoters. &amp;lt;br&amp;gt; &lt;br /&gt;
#finally, deriving a multidimensional unified cis- and trans-regulatory network that describes human-specific and lncRNA-mediated gene regulation in specific cellular states. (Definition of such a network is at: [[Regulatory lncRNAs: &#039;promoting&#039; human uniqueness]]&amp;amp;nbsp;)&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Group members: Leonard Lipovich, Yulia Medvedeva (inviting you to join - please confirm), Vlad Bajic (inviting you to join - please confirm), Jess Mar (inviting you to join - please confirm), and I am also too shy to name (or invite) potential others. Please email me or the F5 list, or please just add yourselves to this page, if you would like to join forces on this.&lt;br /&gt;
&lt;br /&gt;
== Using single direction promoter ti eliminate noise (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Specific transcript (Human) regulation and what are nover TF in human (Haru)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Identification of TFBS by de novo methods (Vlad; Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Predicted homotypic clusters and motif prediction (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Identification fo features of primates specific promoters (?; together with LL)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulation specificity of cells and tissues (Vlad’ s group)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Host pathogen infection relationship; influenza virus, Mycobacteria, Salomonella (Arnab)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Searching for viruses, cryptic viruses (Arnab, mamoon, al, nico)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Deorphanizing transcription factors (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Variation in small RNA population and variation in siRNA machinery (Max)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Cellular restriction of terminal ligases in ubiquitin system (Max)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Papers of individual cells time courses  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== [[Extend rat gene models with CAGEscan]]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Rat gene models sometimes lack a proper 5′&amp;amp;nbsp;UTR. CAGEscan data has been produced using the same RNA (10009-101B8) as the reference FANTOM5 Helicos CAGE library CNhs10612. This experimental data can be used to propose an update of the rat gene models. &lt;br /&gt;
*Group members: [[User:Plessy|Charles Plessy]], Albin Sandelin, other people, please list yourself.&lt;br /&gt;
&lt;br /&gt;
== [[Novel metrics for promoter activity profiles]]  ==&lt;br /&gt;
&lt;br /&gt;
== [[Pathway Fingerprinting]]  ==&lt;br /&gt;
&lt;br /&gt;
== Cellular restriction of epigenomic regulation Erik A. + Andreas Lenn.  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
= Issues: negotiation with sample providers  =&lt;br /&gt;
&lt;br /&gt;
== Encouraged to write paper, but larger stronger papers is perhaps better?  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Talk with collaborator before the datasets is published  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
[[Category:Satellite_paper]]&lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Task_assignments&amp;diff=1553</id>
		<title>Task assignments</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Task_assignments&amp;diff=1553"/>
		<updated>2011-03-03T06:34:15Z</updated>

		<summary type="html">&lt;p&gt;Yulia: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;&#039;&#039;&#039;Task1: Sample acquisition/provision:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Al Forrest, Peter Klinken, Peter Heutink, Claudio Schneider, Kim Summers, Terry Meehan&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt; Sample list - text to Al ASAP&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &amp;amp;nbsp;1. List of missing cellular states on wiki – March 10&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &amp;amp;nbsp;2. Potential sources for missing states – March 10&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &amp;amp;nbsp;3. Acceptance of last snapshots for phase 1 – March 31 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task2: Sample Annotation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Terry Meehan, Win Hide, Tom Freeman, Al Forrest + sample providers&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt; Cell ontology mapping, Tissue ontology mapping&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp;&#039;&#039;Tom’s suggested Sample Annotation &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. UniqueID: Riken tracking number&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Unique_sample_name: Adult_liver.r1 , Tcell_HPC-induced_10h (preferably short, informed by Cell_Ontology)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Species: Hs., Mm., etc.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Sample_Class: Adult_tissue (AT.), Foetal_tissue (FT.), Primary_cell (PC.), Cell_culture (CC.), Time_course (TC-PC.), (TC-CC) etc.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Developmental stage: Adult, Foetal&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 6. Pathology: Normal, disease&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 7. Tissue: Liver, brain, heart etc&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 8. Cell_Ontology (maybe more than one level, to be used in primary sample ordering): Mesenchymal etc, etc&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 9. Cell_type: CO approved name e.g. Monocyte, Smooth_muscle, Intestinal_epithelium etc.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;10. Pertubation: LPS, HPC&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;11. Time: 0, 1h, 2h, 3h etc&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;12. Replicate: r1, r2, r3&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;13. Collection_method: FACS_sorting etc. with short description&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;14. Collection_method_reference: Pubmed_ID, web_address, protocol&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;15. Source: Roslin_Institute&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;16. Primary_contact: Joe_Bloggs&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;17. Email: joe.bloggs@roslin.ed.ac.uk&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;18. Tel: 0044 131 123 4567&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;19. Unique Donor ID&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Annotation of Data freeze 1 samples (cell, tissue – minimum to compare replicates)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Cell ontology – completion by March 15?&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Tissue ontology – March 15 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task3: Mapping:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Timo Lassmann, Geoff Faulkner&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; BAM&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; CTSS&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones: &amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Rescuing assessment (March 5)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Decision (March 7)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Genome version agreement – comment on pseudoautosomal regions&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Mapping of Data freeze 1 (GENAS??) &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task4: Tag clustering:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names: &amp;lt;/u&amp;gt;Piero Carninci, Cesare Furlanello, Piotr Balwierz, Martin Taylor, Martin Frith, Kawaji-san, Boris Lenhard, Albin Sandelin - clustering. David Hume, Ben Brown, Al Forrest - assessment&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Clusters defined as regions on a genome with strand, start, stop, peak and build(Bed?)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Intersect of the defined regions as an expression matrix/table across all samples (ie. intersect of clusters with expression in all libraries) &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Possibly.. intersected CTSS file of same regions to allow study of independent peak regulation&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Peak rec&amp;lt;br&amp;gt;&#039;&#039;&amp;amp;nbsp;Tom’s suggestion&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; Data Matrix Annotation&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; To be provided by Riken as raw counts (.raw) and tags per million (.tpm) but ultimately data may be normalised by other methods (.xxx)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. UniqueID: Gene Level (MGD, HGNC ID), Transcript or promoter level (ABC1.1, ABC1.2 etc), ncRNA (Leonard’s ID)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Class: Gene_promoter, ncRNA_promoter, other&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Chromosomal_location: e.g. alignment range, promoter peak&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Chromosome: Chr1&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Associated_seqs: refseq, ensembl_gene/transcript, ncRNA_ref&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 6. Other_associations: KEGG, GO etc&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;1. Agreement on format and training/tuning/assessment data and metrics (March 5)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;2. Competitive tracks available – March 25&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;3. Assessment – April 5&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp;4. Run over paper 1 data freeze – mid April &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task5: State enriched(expression weighted) motif predictions (ab-initio and known): &amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt;Vlad Bajic, Michiel de Hoon, Boris Lenhard, Kenneth Baiulie, Timo Lassmann, Piotr Balwierz, Yulia Medvedeva&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats: &amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Ranked list of motifs enriched in each state for release 010&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Bed file(or similar) with actual predictions for release 010&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. As above on FREEZE 1 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task5: [[Tag Cluster Annotation]]:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Piero Carninci, Laurens Wilming, Timo Lassmann, Richard Baldarelli, Juha Kere, Leonard Lipovich(long ncRNA promoters, sense-antisense pair promoters, bidirectional promoters), Boris Lenhard(enhancers), Alison Meynert, Yulia Medvedeva (CpG islands, DNA methylation, Repeats)&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats: &amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Agreement on annotations to use (now?) (I will supply the global human lncRNAome and sense-antisense coordinates for the annotation. - LL)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Annotation of release 009 clusters using agreed strategy – available ASAP&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Annotation of data freeze 1 (ASAP after the clusters are provided) &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task6: Cross species promoter mapping:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Martin Taylor, Colin Semple, Vlad Bajic, Peter Heutink, Max Burroughs, Soichi Ogishima, Leonard Lipovich (if we are doing non-conserved promoters)&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&amp;amp;nbsp;&amp;amp;nbsp;Martins Taylor&#039;s suggested format&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_tag_cluster_ID &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_genome_assembly_ID&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_chrom &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_refPos &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species1_strand&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_tag_cluster_ID&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_genome_assembly_ID&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_chrom&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_refPos&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; species2_strand&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projection_method (a list of rule sets whose criteria were met*)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projection_distance (a measure of confidence in the projection)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projection_result (e.g. species1_rescue, species2_rescue....)&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; *e.g. identical projected modal tag position, quantile overlap of&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; projected tag cluster distributions, cluster coordinate overlap.&#039;&#039; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Prediction/mapping of human promoters using mouse data (April 15)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Validation on the matched 10-30 human-mouse pairs (ie predict with mouse and check with actual human data). Assessment of strategy.&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Prediction of human counterpart promoters for the rare mouse cells that we have collected (eg. intestinal stem cells, inner ear hair cells etc.). &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Do we need a preliminary count of nonconserved human promoters (those absent from the other 4 F5 species)? (LL)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task7: Expression visualization (gene level AND TSScluster level):&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Tom Freeman,Kenneth Baillie, Carsten Daub, Win Hide, Boris Lenhard, Albin Sandelin&amp;amp;nbsp;&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats&amp;lt;/u&amp;gt;: potential figures for displaying relationship of samples based on expression clustering&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Gene level information humanx3(tissue, cell line, primary cells) -&amp;amp;gt; Biolayout webstart&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Distance matrix, genes and pathways that separate each state - Win Hide &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task8: Promoter level expression analysis (differentially expressed genes/markers/transcription factors/ncRNAs):&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Piero Carninci, Al Forrest, Albin Sandelin, Vlad Bajic, Yulia Medvedeva, Hideya Kawaji, Ben Brown, Tom Freeman, Harukazu Suzuki, Colin Semple, David Human, Cesare Furlanello, Kenneth Bailie and Jess Mar, Timothy Ravasi, Leonard Lipovich&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;1. Agreement on metric for specificity/enrichment – entropy Ravasi March 5&amp;lt;br&amp;gt;2. Ranked list of most specific TFs for each state&amp;lt;br&amp;gt;3. Ranked list of ncRNAs specific for each state (incl. curated lncRNAs that define specific steady states -LL)&amp;lt;br&amp;gt;4. Ranked list of all genes specific for each state &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task9: Expression data mining:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Carlo, Tim&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt; &lt;br /&gt;
&lt;br /&gt;
1. Explore the data set using maximum curvilinearity methods and see if it helps classify the layers &lt;br /&gt;
&lt;br /&gt;
Boosting? SVMs? &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task10: Motif activity and TF expression integration (including deorphanization):&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Vlad Bajic, Michiel de Hoon, Piotr Balwierz, Yulia Medvedeva, Matthias Harbers, Al Forrest&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;1. Expanding Motifs&amp;lt;br&amp;gt;2. Core predicted set&amp;lt;br&amp;gt;3. Attempt at integrating list of sample enriched TFs and sample enriched motifs.&amp;lt;br&amp;gt;4. Prioritized orphan associations for validation &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task10:&amp;amp;nbsp;Sanity check:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Al Forrest, Piero Carninci&amp;lt;br&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;br&amp;gt;1. Assessment of strategy above&amp;lt;br&amp;gt;2. OK or repeat from step XYZ &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&#039;&#039;&#039;Task11: Data dissemination and nomenclature:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names: &amp;lt;/u&amp;gt;Win Hide, David Hume, Piero Carninci, Richard Baldarelli, Vlad Bajic, Tom Freeman, Yoshihide Hayashizaki, John Quackenbush, Laurens, Terry Meehan, Hideya Kawaji, Timo Lassmann, Albin Sandelin&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; ‘Promoter’ – dissemination&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; ‘expression’ – dissemination&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; ‘cell/sample’ – dissemination?&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Agreement on strategy&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Agreement on formats&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Agreement on third party data repositories (especially UCSC and Ensembl)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Core promoters with accessions and link to our data nomenclature &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task12: ChipSeq Validation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names&amp;lt;/u&amp;gt;: RIKEN OSC, Tim Ravasi, Al Forrest, Matthias Harbers, WP9&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;lt;u&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;lt;/u&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Target selection – considering cell type, predictions, chip grade antibody, impact&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Assessment of targets&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Motif finding&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Public chip-seq data &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task13: Public data integration:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Vlad, David, Yulia, Louise, Thomas, Terry, Matthias &amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;u&amp;gt;Milestones:&amp;lt;/u&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Extract public Chip-seq data &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Extract public mouse KO &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Extract edges from literature mining (vlad) &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. Extract in-situ mapping from Allen brain atlas, eurexpress, emage &lt;br /&gt;
&lt;br /&gt;
&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Extract localization information from human protein atlas&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;Task14: KDCAGE Validation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; RIKEN OSC, WP9 (intersection of chip-seq known and )&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Target selection – considering cell type, predictions, impact&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. Assessment of targets&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Motif finding &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&#039;&#039;&#039;Task15: In-situ validation: (likely very late in project)&amp;lt;br&amp;gt;&#039;&#039;&#039;Committed names: Juha? Peter H? Silivia, &amp;lt;br&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; 1. Target selection &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; 2. In-situ on a small set of human samples&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; 3. Likely very late in the project&amp;lt;br&amp;gt; &amp;lt;br&amp;gt;&#039;&#039;&#039;Task16: Paper4 - Cross species network conservation:&amp;lt;br&amp;gt;&#039;&#039;&#039;&amp;lt;u&amp;gt;Committed names:&amp;lt;/u&amp;gt; Al Forrest, Martin Taylor, Peter Heutink, Michiel de Hoon, Mamoon Rashid, Colin Semple, Vlad Bajic, Max Burroughs, Soichi Ogishima, Leonard Lipovich&amp;lt;br&amp;gt;&amp;lt;u&amp;gt;Output requirements/formats:&amp;lt;br&amp;gt;Milestones:&amp;lt;/u&amp;gt;&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 1. Gene level ortholog pairs (CDS matching)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 2. TSS cluster level ortholog pairs (genome matching)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 3. Ortholog expression correlations (use expression data from above group, and ortholog mappings from 1 and 2)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 4. State specific motif enrichment (conservation independent)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 5. Tf state specific expression&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 6. siRNA KD of SMC specific TFs in multiple species&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 7. Potential chip-seq&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 8. Availability of Macaque samples? Aortic SMC, hepatocytes, Bone marrow MSCs&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 9. Macrophages across all species? Peripheral blood (PBMCs)&amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 10. Integration of cis-networks (bidirectional promoters; TF to lncRNA; antisense lncRNA to sense mRNA gene) with existing networks -LL &amp;lt;br&amp;gt;&amp;amp;nbsp;&amp;amp;nbsp; &amp;amp;nbsp; 11. Examples of specific non-conserved networks -LL &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt;&amp;lt;br&amp;gt;&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Tag_Cluster_Annotation&amp;diff=1552</id>
		<title>Tag Cluster Annotation</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Tag_Cluster_Annotation&amp;diff=1552"/>
		<updated>2011-03-03T06:29:50Z</updated>

		<summary type="html">&lt;p&gt;Yulia: /* Committed names */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;==Committed names==&lt;br /&gt;
* Piero Carninci&lt;br /&gt;
* Laurens Wilming&lt;br /&gt;
* Timo Lassmann&lt;br /&gt;
* Richard Baldarelli&lt;br /&gt;
* Juha Kere&lt;br /&gt;
* Leonard Lipovich(long ncRNA promoters, sense-antisense pair promoters, bidirectional promoters, global human lncRNAome and sense-antisense coordinates)&lt;br /&gt;
* Boris Lenhard(enhancers)&lt;br /&gt;
* [[User:ameynert|Alison Meynert]] (Ensembl gene models)&lt;br /&gt;
* Sarah Djebali&lt;br /&gt;
* Yulia Medvedeva (CpG islands, DNA methylation, Repeats)&lt;br /&gt;
&lt;br /&gt;
==Annotations &amp;amp; assignments==&lt;br /&gt;
&lt;br /&gt;
&#039;&#039;&#039;NB: we will need to be careful about 0-based and 1-based coordinates&#039;&#039;&#039;&lt;br /&gt;
&lt;br /&gt;
Given the majority of people in FANTOM5 seem to be UCSC focused, propose we use 0-based UCSC format with &#039;chr&#039; prefix. Any Ensembl or other 1-based annotations will need to be adjusted in the output and a note added to the flat file headers/README.&lt;br /&gt;
&lt;br /&gt;
==Output requirements/formats==&lt;br /&gt;
&lt;br /&gt;
===Proposal - flat file format===&lt;br /&gt;
&lt;br /&gt;
[http://fantom.gsc.riken.jp/4/download/Tables/doc/ OSCtable] format tab-delimited file, separate files for each species, could also be separate files per annotation class, but should be able to mash together all files for a species into one without re-formatting.&lt;br /&gt;
&lt;br /&gt;
Here is an initial sketch of a possible flat-file format (scroll right to see it all):&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pre&amp;gt;&lt;br /&gt;
##&lt;br /&gt;
## Contact name =  Ann Otator&lt;br /&gt;
## Contact e-mail = ann.otator@institute&lt;br /&gt;
## Description = General annotations (or could be just e.g. Ensembl gene models, lncRNAs, enhancers)&lt;br /&gt;
## Species = Homo sapiens&lt;br /&gt;
## NCBI taxon id = 9606&lt;br /&gt;
## Release = FANTOM5 UPDATE_009&lt;br /&gt;
## &lt;br /&gt;
Tag_cluster_id Library_id  Annotation_class      Annotation_type      Annotation_id   Distance Chr  Tag_cluster_pos Tag_cluster_strand Annotation_start Annotation_end Annotation_strand&lt;br /&gt;
TSC000001      CNhs11772   CORE_PROMOTER         ENSEMBL_TRANSCRIPT   ENST00000000001 -30      chr1 1234153         +                  1234183          1238888        +     &lt;br /&gt;
TSC000002      .           3_PRIME_UTR           UCSC_TRANSCRIPT      GENE1           .        chr2 1234124         +                  1234124          1289193        +&lt;br /&gt;
TSC000003      .           CORE_PROMOTER         LONG_NC_RNA          LEONARD01       -2       chr3 4848484         -                  4848400          4848482        -&lt;br /&gt;
TSC000004      CNhs11334   LONG_RANGE_REGULATION VISTA_ENHANCER       VISTA001        .        chr4 3893493         +                  3893400          3893499        -&lt;br /&gt;
TSC000005      .           EXTENDED_PROMOTER     ENSEMBL_TRANSCRIPT   ENST00000000002 -503     chr5 3485928         +                  3482000          3486431        -&lt;br /&gt;
&amp;lt;/pre&amp;gt;&lt;br /&gt;
&lt;br /&gt;
If the library id is given, the tag cluster is associated with that specific library; otherwise, it is associated with the aggregate of all libraries. It is possible that some annotations will not be required on a per-library basis.&lt;br /&gt;
&lt;br /&gt;
Some types of annotation (e.g. core promoter, extended promoter) we will want to include the distance from the tag cluster reference position to the annotation position (e.g. annotated protein-coding gene TSS). For other types (e.g. 3&#039; UTR, exonic), it&#039;s enough to know that the tag cluster reference position overlaps that annotation, and the distance can be unspecified.&lt;br /&gt;
&lt;br /&gt;
===Proposal - MySQL database schema===&lt;br /&gt;
&lt;br /&gt;
Is this something that people would find useful? Here&#039;s a very de-normalized schema - another option is to have one table per species and just follow the flat-file format.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pre&amp;gt;&lt;br /&gt;
CREATE TABLE library (&lt;br /&gt;
&lt;br /&gt;
  library_id  VARCHAR(9) NOT NULL,&lt;br /&gt;
  species     VARCHAR(40) NOT NULL,&lt;br /&gt;
  taxon_id    INT(10) UNSIGNED NOT NULL,&lt;br /&gt;
  source      ENUM(&#039;primary cell&#039;, &#039;cell line&#039;, &#039;tissue&#039;, &#039;timecourse&#039;, &#039;quality control&#039;) NOT NULL,&lt;br /&gt;
  description VARCHAR(100) NOT NULL,&lt;br /&gt;
&lt;br /&gt;
  PRIMARY KEY (library_id)&lt;br /&gt;
&lt;br /&gt;
);&lt;br /&gt;
&lt;br /&gt;
CREATE TABLE annotation (&lt;br /&gt;
&lt;br /&gt;
  annotation_id INT(10) UNSIGNED NOT NULL,&lt;br /&gt;
  taxon_id      INT(10) UNSIGNED NOT NULL,&lt;br /&gt;
  class         VARCHAR(40) NOT NULL,&lt;br /&gt;
  source        VARCHAR(40) NOT NULL,&lt;br /&gt;
  type          VARCHAR(40) NOT NULL,&lt;br /&gt;
  external_id   VARCHAR(40) NOT NULL,&lt;br /&gt;
  chr           VARCHAR(40) NOT NULL,&lt;br /&gt;
  pos           VARCHAR(40) NOT NULL,&lt;br /&gt;
&lt;br /&gt;
  PRIMARY KEY (annotation_id),&lt;br /&gt;
  KEY annotation_idx (class, source, type, external_id),&lt;br /&gt;
  KEY location_idx (chr, pos)&lt;br /&gt;
&lt;br /&gt;
);&lt;br /&gt;
&lt;br /&gt;
CREATE TABLE tag_cluster (&lt;br /&gt;
&lt;br /&gt;
  library_id     VARCHAR(9) NOT NULL,&lt;br /&gt;
  tag_cluster_id VARCHAR(40) NOT NULL,&lt;br /&gt;
  chr            VARCHAR(40) NOT NULL,&lt;br /&gt;
  pos            INT(10) UNSIGNED NOT NULL,&lt;br /&gt;
&lt;br /&gt;
  PRIMARY KEY (tag_cluster_id)&lt;br /&gt;
  KEY location_idx (chr, pos)&lt;br /&gt;
&lt;br /&gt;
);&lt;br /&gt;
&lt;br /&gt;
CREATE TABLE tag_cluster_annotation (&lt;br /&gt;
&lt;br /&gt;
  annotation_id  INT(10) UNSIGNED NOT NULL,&lt;br /&gt;
  tag_cluster_id VARCHAR(40) NOT NULL,&lt;br /&gt;
&lt;br /&gt;
  KEY annotation_idx (annotation_id),&lt;br /&gt;
  KEY tag_cluster_idx (tag_cluster_id)&lt;br /&gt;
);&lt;br /&gt;
&amp;lt;/pre&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Milestones==&lt;br /&gt;
# Agreement on annotations to use ([[Media:Annotation_ncRNA_and_promoters-discussion_group_F5.pdf|Working group notes from Piero]])&lt;br /&gt;
#*Set out annotation list and any definitions (e.g. core promoter vs. extended promoter) on this wiki page&lt;br /&gt;
#*Assignment of annotation types to participants&lt;br /&gt;
#*Agreement on output format - ASAP&lt;br /&gt;
# Annotation of release 009 clusters using agreed strategy &lt;br /&gt;
#*Are we waiting on the results of the tag cluster competition or is there a test set of clusters that we can start working on?&lt;br /&gt;
# Annotation of data freeze 1 - ASAP after freeze&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
	<entry>
		<id>http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_papers&amp;diff=1517</id>
		<title>Satellite papers</title>
		<link rel="alternate" type="text/html" href="http://fantom5-collaboration.gsc.riken.jp/wiki/index.php?title=Satellite_papers&amp;diff=1517"/>
		<updated>2011-03-01T16:12:47Z</updated>

		<summary type="html">&lt;p&gt;Yulia: /* Methylation effect on TFBS and expression (Yulia) */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;= Instructions  =&lt;br /&gt;
&lt;br /&gt;
Below you can find the list of satellite paper proposals collected in the February meeting. Please add the following information to each of the proposals &lt;br /&gt;
&lt;br /&gt;
*Check the title &lt;br /&gt;
*provide brief outline of the proposal &lt;br /&gt;
*add/remove your name in case you are interested to work on this satellite paper&lt;br /&gt;
&lt;br /&gt;
Proposal for satellites papers 2/25/2011 Purpose: list up potential satellites; avoid redundancies, make better papers Figure out potential titles to discuss how to negotiate with specific journals. &lt;br /&gt;
&lt;br /&gt;
Add a set of sentences (mini abstract) on the wiki and write an abstract &lt;br /&gt;
&lt;br /&gt;
= Bioinformatics analysis methods  =&lt;br /&gt;
&lt;br /&gt;
== Normalization and clustering issues  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: Tom Freeman&lt;br /&gt;
&lt;br /&gt;
== Modulation of gene expression (Jess Mar)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Expanding transcriptional reg. networks (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Tag clusterin in helicos CAGE (Cesare)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Computation methods for networks comparisons]] (cesare)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Tool to make the promoter subsets at will (do not ask us datasets!) (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Delve tag mapping paper (Timo L)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Methods paper on Delve: a probabilistic read mapper. &lt;br /&gt;
*Group members: Timo Lassmann, Carsten Daub&lt;br /&gt;
&lt;br /&gt;
== Classification of CAGE peaks (Timo L)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Deeply sequenced CAGE libraries capture signals on many non-promoter regions. The purpose of this paper is to describe a strategy to separate TSS from non-TSS CAGE peaks (see: [[media:CAGE_classification.pdf]]). Preliminary work suggest that further sub-classicifation of promoters based on the shape of the CAGE signal is possible (see: [[media:Brood_october_2010.pdf]]).&lt;br /&gt;
*Group members: Timo Lassmann, Ben Brown, Colin Semple&lt;br /&gt;
&lt;br /&gt;
== Peak finder-noise elimination contest paper (all runners)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Genomics-broad scale analysis  =&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Alternative TSS in cancer relevant to biomarkers (Win Hide)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Impact of alternative promoters on biology of genes (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== How much do we need to sequence? Complexity of the transcriptome (Albin)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Revised analysis of zinc finger proteins (Tim Ravasi, David Hume)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Identification of distal regulation elements: role of enhancers in differentiation (Carsten, Boris, Ana P, Jose, YH)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== miRNA promoters (Hideya K, Eivind Al, )  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== CAGE tags on Pigs: Gain and loss of promoters (David Hume) [satellite of the pig genome]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulatory transcription outside canonical promoters (Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Transcription initiation in embryo development (Boris)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Promoters with multiple TSS configuration-multiple ways to use the same promoters (Boris, Kawaji)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Link Fantom 5 to genetic datasets (Peter Heutink; Juha K)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Methylation effect on TFBS and expression (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: It&#039;s commonly accepted that DNA methylation of a promoter repress transcription of this gene in normal tissues. Recently, a class of actively expressed genes having relatively methylated promoters has been discovered. The purpose of this research is to explore the idea that DNA methylation effects CG-rich TFBS, preventing TF from binding to DNA, and therefore represses transcription. &lt;br /&gt;
 &lt;br /&gt;
*Group members: Yulia Medvedeva&lt;br /&gt;
&lt;br /&gt;
== Comparison of different types/feature of promoters and genome features to study specific differences (Yulia)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Multiple genomics analysis on multiple datasets (Haru) Extension of the validation?  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Prediction of cell transformation states (Win Hide)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Convergent evolution of retrotransposon promoters (Geoff)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Following the model for the anti-apoptosis gene NAIP (Romanish et al., PLoS Genetics, 2007), we will start by screening the mouse and human genomes for instances where two different retrotransposons occupy the same or similar location in protein-coding genes (e.g. an Alu in human, a B2 in mouse). If this happens frequently enough to be interesting, we will overlay the F5 data onto the &amp;quot;convergent&amp;quot; retrotransposons to see how many are transcribed, what role they may have in regulation (e.g. Lunyak et al., Science, 2007) and if the events are more common for some pathways than others (e.g. in embryogenesis or brain development).&amp;lt;br&amp;gt;&lt;br /&gt;
*Group members: Geoff, Piero&amp;lt;br&amp;gt;&lt;br /&gt;
&lt;br /&gt;
== Alternative TSS and alternative splicing (Nicolas)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Chimaeric RNA and 3D structure (if it works) (Nicolas)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Annotation of genes involved in biochemical, metabolic processes and signature for processes-for instance signature for tumors – expression based GO terms (Tom Freeman) (Richard Baldarelli, Jackson and GO groups) (David Hume) ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
&amp;lt;br&amp;gt; &lt;br /&gt;
&lt;br /&gt;
= Blood group: fill in the holes, more discussion  =&lt;br /&gt;
&lt;br /&gt;
== Granulopoiesis analysis (Andreas Lenn.)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Cellular restriction of epigenomic regulation Erik A. + Andreas Lenn.  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Eritropoiesis (Peter K)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== HSC (Sugiyama san)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Macrophages (DH)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Subpopulations T cells and monocytes (Michael R)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Brain groups 4 papers Other priority areas in brain: discuss other brain and diseases (YH)  =&lt;br /&gt;
&lt;br /&gt;
== Evolution gene expression in vertebrates Martin + Peter Heutink  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Study the evolution of gene expression combining insights from each of the following: &lt;br /&gt;
** Gene/transcript level changes in expression (and estimating it&#039;s constraint/diversification). &lt;br /&gt;
** TSS/promoter turnover: orthologous genes using non-orthologous promoters, or changes in promoter-preference for one cell type between species. &lt;br /&gt;
** Sequence evolution of core promoters and distant regulatory blocks correlated with changes in gene expression.&lt;br /&gt;
* Focus of the paper on the well matched cells between ((Human, (Macaque?)),(Mouse, Rat),Dog),Chicken) for which we have hCAGE data. (Cell types: Hepatocytes, Aortic smooth muscle cells, mesenchymal stem cells).&lt;br /&gt;
*Group members: Martin Taylor, Peter Heutink, Alison Meynert &lt;br /&gt;
*Details: [[Evolution in gene expression]].&lt;br /&gt;
&lt;br /&gt;
== Transcriptional constrains seq evolution [Martin+Michiel talk]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: [Michiel:] Network analysis across organisms &amp;amp;amp; evolution of regulatory networks, in particular of developmental networks. Are there any subnetworks particularly conserved between organisms? What does this tell us about the functional importance and relevance of specific subnetworks? Do we see any recurring patterns in the network (Uri Alon-type feed-forward loops)? What are the conservation patterns and rates of divergence of transcription factors and specific regulatory relations? Do we see turnover of TFBSs, or do we see conservation of TFBSs in alignments? This can be applied specifically to brain, or more generally to all CAGE samples. TFBS prediction in Neanderthal compared to Homo sapiens would be really cool. &lt;br /&gt;
*Group members: Martin, Michiel, Peter Heutink &lt;br /&gt;
*Martin&#039;s and Michiel&#039;s idea for this paper may overlap or may be complementary to each other; we need to discuss this. This may end up as two satellite papers or one integrated one.&lt;br /&gt;
&lt;br /&gt;
== Tfbs turnover in liver (integrate with ChIP seq) Martin  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Integration of cross-species ChIP-seq data in liver with proximal CAGE tag cluster responses in the same species. Data on liver ChIP-seq for the transcription factors HNF1A and CEBPA in human/mouse/dog/(chicken) Schmidt et al, Science 2010 has been obtained. The questions we can address with this study are:      &lt;br /&gt;
** Are conserved binding sites more likely than non-conserved sites to elicit a local, hepatocyte specific ranscriptional response? (Use CEBPA non-expressing cells to generate a background model of proximal transcriptional responses). This could be used to estimate &amp;quot;functional turnover&amp;quot; as opposed to the &amp;quot;binding turnover&amp;quot; as reported by Duncan Odom.&lt;br /&gt;
** Does hepatocyte specific expression (around binding sites) segregate through species lineages with the experimentally defined binding site?&lt;br /&gt;
** If there is apparent turn-over of binding sites, is the pattern of local responsive transcription conserved?&lt;br /&gt;
** Do we see conservation of hepatocyte specific transcriptional responses even in the absence of binding site conservation? &lt;br /&gt;
*Group members: Martin Taylor, Alison Meynert&lt;br /&gt;
&lt;br /&gt;
== Disease paper (brain): human post mortem, … comparison healthy-disease Peter Heutink + Gustincich group  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Rett syndrome and visual cortex Alka  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Genomic architecture in 3 genes involved in Rett syndrome Alka  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Genomic architecture of neurodegenerative disease (Gustincich talk P.H., etc.)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
= Others  =&lt;br /&gt;
&lt;br /&gt;
== [[Olfactory receptors]]  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: Promoters of [[Olfactory receptors]] (ORs) are still poorly documented. We have an unpublished promoter list for mouse, and CAGE libraries from human olfactory mucosa will be made. We will identify the promoters of the human ORs and analyse their structure. Many ORs have [[Alternative Promoters|alternative promoters]] and this is a potential example for the promotorome paper. Human-specific OR promoters might be found. There is evidence of expression of the ORs outside the mouse and human olfactory mucosa, and this satellite paper will report this. Experiments to find a ligand and propose a function may be carried out. More information on the page: [[Olfactory receptors]]. &lt;br /&gt;
*Group members: [[User:Plessy|Charles Plessy]], Giovanni Pascarella, Stefano Gustincich and others, but I am too shy to add their name without asking.&lt;br /&gt;
&lt;br /&gt;
== Cell-Cell communicatome (Al forrest)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Drugable cells: drug targets (Al Forrest)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Definition of stem or precursors relationship (Claudio Schneider)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Gene regulation in cells of connective tissues (Vlad, Kim)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Transdifferentiation and network rewiring (Haru; WP6 + others) POTENTIAL main paper for later stage  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Network in cancer (Rama, win’s group)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Regulatory network in cell lineage tree (Carsten wp5)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Determination of conserved CAGE (Vlad)  ==&lt;br /&gt;
&lt;br /&gt;
*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
&lt;br /&gt;
== Promoting human uniqueness: human-specific promoters of regulatory lncRNA genes drive cis- and trans-regulation. (LL)  ==&lt;br /&gt;
&lt;br /&gt;
*More information at: [[Regulatory lncRNAs: &#039;promoting&#039; human uniqueness]]&lt;br /&gt;
*Outline: TBD &lt;br /&gt;
*Group members: Leonard Lipovich, Yulia Medvedeva (inviting you to join - please confirm), Vlad Bajic (inviting you to join - please confirm), Jess Mar (inviting you to join - please confirm), and I am also too shy to name (or invite) potential others. Please email me or the F5 list, or please just add yourselves to this page, if you would like to work on this.&lt;br /&gt;
* Anticipated ABSTRACT (Big Picture of what we will likely see, with actual numbers coming later; XXX, YYY etc are placeholders for the actual numbers). &lt;br /&gt;
In FANTOM3, we learned that complex loci -- sense-antisense pairs, bidirectional promoters, and gene chains -- are prevalent in mammalian genomes. These complex loci often contain long non-coding RNA (lncRNA) genes which have the potential to cis-regulate protein-coding genes, but whose sequences and genomic structures are often not conserved between human and mouse (Katayama et al 2005; Engstrom et al 2006). The specific contribution of non-conserved sequences to regulation at complex loci has remained obscure. To quantify and characterize the functional significance of non-conserved lncRNA regulation, we have used the FANTOM5 human CAGE Promoterome to catalog: XXXXXX Transcription Start Sites (TSS) in single-copy human genomic sequences unalignable to mouse, rat, dog/pig(?), and chicken; and the FANTOM5 human CAGEscan data to define XXXXX additional human TSS-s inside primate-specific Alu repeats (all collectively defined as &amp;quot;human-specific TSS-s&amp;quot;). We computed the intersection of these human-specific TSSs with: XXXX nonredundant lncRNA genes from our cDNA-supported lncRNA catalog and from other groups; XXXX human bidirectional promoters of lncRNA-mRNA gene pairs; and ~2800 lncRNA-mRNA sense-antisense pairs identified by our sense-antisense discovery pipeline. XXXXX human-specific TSS-s belonged to standalone lncRNA genes, YYYYY to lncRNA genes in lncRNA-mRNA sense-antisense and bidirectional-promoter pairs, and ZZZZZ to lncRNA genes in chains; therefore, {YYYYY+ZZZZZ} (##% of total) human-specific TSS-s are associated with lncRNA genes that may cis-regulate protein-coding genes. Here, we apply the FANTOM5 human tissue and primary cell culture resource to describe human spatiotemporal lncRNA-mRNA co-expression in gene pairs and chains, finding that XXX co-expressed lncRNA-mRNA pairs depend on human-specific lncRNA TSS-s. Comparative manual annotation of mouse transcriptome data reveals that XXX of the orthologous mouse mRNAs lack any evidence of adjacent or antisense lncRNA transcription, suggesting that the corresponding CAGE-supported human lncRNA TSS-s are indeed human-specific. We infer XXX specific transcriptional cis-regulatory networks consisting of known transcription factors, human-specific lncRNA promoters, lncRNAs, and mRNAs regulated by the lncRNAs. Protein-coding genes in these cis-networks are preferentially expressed in specific {WHICH?} tissues and are enriched in specific {WHICH?} functions {INSERT RESULTS HERE: BRAIN? SYNAPTIC PLASTICITY? RELEVANCE TO HIGHER-ORDER BEHAVIORS??}, defining a unique functional space occupied by the non-conserved human lncRNA-mRNA cis-co-regulome. Cell-culture-based reverse-genetic interrogation of {SELECTED} lncRNAs with human-specific TSS-s, by RNAi and overexpression, confirms both the cis-regulatory potential of lncRNAs with human-specific promoters to modulate their genomic neighbor genes and the trans-regulatory effects of such modulation on the rest of the protein-coding transcriptome (NOTE - this is only possible if OSC can help us with validations). These results indicate that, while the genomics community primarily pursues the function of multispecies conserved sequences, interspecies gene structure differences caused by non-conserved lncRNA promoters are functional in evolutionary lineage-specific regulation.&lt;br /&gt;
== Using single direction promoter ti eliminate noise (Yulia)  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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== Specific transcript (Human) regulation and what are nover TF in human (Haru)  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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== Identification of TFBS by de novo methods (Vlad; Boris)  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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== Predicted homotypic clusters and motif prediction (Yulia)  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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== Identification fo features of primates specific promoters (?; together with LL)  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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== Regulation specificity of cells and tissues (Vlad’ s group)  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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== Host pathogen infection relationship; influenza virus, Mycobacteria, Salomonella (Arnab)  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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== Searching for viruses, cryptic viruses (Arnab, mamoon, al, nico)  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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== Deorphanizing transcription factors (Vlad)  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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== Variation in small RNA population and variation in siRNA machinery (Max)  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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== Cellular restriction of terminal ligases in ubiquitin system (Max)  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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== Papers of individual cells time courses  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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== [[Extend rat gene models with CAGEscan]]  ==&lt;br /&gt;
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*Outline: Rat gene models sometimes lack a proper 5′&amp;amp;nbsp;UTR. CAGEscan data has been produced using the same RNA (10009-101B8) as the reference FANTOM5 Helicos CAGE library CNhs10612. This experimental data can be used to propose an update of the rat gene models. &lt;br /&gt;
*Group members: [[User:Plessy|Charles Plessy]], Albin Sandelin, other people, please list yourself.&lt;br /&gt;
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== [[Novel metrics for promoter activity profiles]] ==&lt;br /&gt;
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== [[Pathway Fingerprinting]] ==&lt;br /&gt;
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= Issues: negotiation with sample providers  =&lt;br /&gt;
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== Encouraged to write paper, but larger stronger papers is perhaps better?  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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== Talk with collaborator before the datasets is published  ==&lt;br /&gt;
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*Outline: bla &lt;br /&gt;
*Group members: xxx, yyy, zzz&lt;br /&gt;
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[[Category:Satellite_paper]]&lt;/div&gt;</summary>
		<author><name>Yulia</name></author>
	</entry>
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