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Control of Embryonic Stem Cell State by Mediator and Cohesin (Illumina ChIP-Seq data)

ABSTRACT: The key transcription factors that control the embryonic stem cell gene expression program have been identified, but how they function to implement this program is not well understood. While screening for genes essential for maintenance of ES cell state, we identified many components of the Mediator and Cohesin complexes. Mediator and Cohesin were found to physically and functionally connect the enhancers and core promoters of active genes. An ES cell Mediator complex was found to copurify with Cohesin and its loading factor Nipbl, and normal levels of these proteins were essential for expression of the genes they occupy and for maintenance of ES cell state. See associated publication.

ORGANISM(S): Mus musculus

SUBMITTER: Richard Young

PROVIDER: E-GEOD-22562 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Mediator and cohesin connect gene expression and chromatin architecture.

Kagey Michael H MH Newman Jamie J JJ Bilodeau Steve S Zhan Ye Y Orlando David A DA van Berkum Nynke L NL Ebmeier Christopher C CC Goossens Jesse J Rahl Peter B PB Levine Stuart S SS Taatjes Dylan J DJ Dekker Job J Young Richard A RA

Nature 20100818 7314

Transcription factors control cell-specific gene expression programs through interactions with diverse coactivators and the transcription apparatus. Gene activation may involve DNA loop formation between enhancer-bound transcription factors and the transcription apparatus at the core promoter, but this process is not well understood. Here we report that mediator and cohesin physically and functionally connect the enhancers and core promoters of active genes in murine embryonic stem cells. Mediat ...[more]

PMID: 20720539

Similar Datasets

Control of Embryonic Stem Cell State by Mediator and Cohesin

Project description:This SuperSeries is composed of the following subset Series: GSE22556: Control of Embryonic Stem Cell State by Mediator and Cohesin (Agilent gene expression data) GSE22562: Control of Embryonic Stem Cell State by Mediator and Cohesin (Illumina ChIP-Seq data) Refer to individual Series

2010-08-11 | E-GEOD-22557 | biostudies-arrayexpress

Transcription factor binding in human embryonic stem cells

Project description:Cohesin interacts with Mediator to link the enhancers and core promoters of actively transcribed genes bound by RNA polymerase II. Activin signaling directs human embryonic stem cells to differentiate into endoderm. ChIP-seq was performed to determine the gene targets of these factors in human embryonic stem cells. Human ES cells were grown without feeders using mTESR1. ChIP-seq was performed against RNA Pol2, Cohesin subunits (Smc1 and Smc3) and IgG for cells grown in mTESR1. Cells were differentiated into endoderm after resting for 24 hours in RMPI-B27 (0hr), and then treating with 50 ng/ml Activin A for two hours (2hr) and 48 hours (48hr). DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing.

2012-03-17 | E-GEOD-36578 | biostudies-arrayexpress

ChIP-Seq for NIPBL for SMC1 in human lymphoblastoid cells (hLCLs)

Project description:The gene expression program is regulated by a cell-type specific chromosome architecture. The connection between enhancer and promoter regions is dependent on a protein complex containing Nipbl, Mediator and Cohesin. To gain insights into the chromosome architecture of human differentiated cells, we profiled NIPBL and SMC1 in lymphoblastoid cells (LCLs). DNA was enriched from hLCLs and chromatin immunoprecipitations (ChIPs) were analyzed by Solexa sequencing. ChIPs were performed using an antibody against NIPBL and SMC1. Whole cell extract is provided for background.

2012-06-01 | E-GEOD-38395 | biostudies-arrayexpress

Transcription-associated Loading and Translocation of Condensin II on Chromosome Arms in Embryonic Stem Cells (flavopiridol ChIP-Seq)

Project description:Condensin molecules are loaded onto the genome to mediate essential changes in chromosome condensation during mitosis, but it is not clear why there are two forms of vertebrate condensin that become differentially distributed on chromosomes. We report here that condensin II, the form of condensin present in the nucleus throughout the cell cycle, functions specifically at active genes. Condensin II is loaded at transcriptionally active promoters in embryonic stem cells (ESCs), migrates through these genes in a transcription-dependent fashion and accumulates in transcription termination regions. Unlike cohesin, which is also loaded at active promoters, condensin II has little influence on transcription. We conclude that condensin II is loaded and distributed across actively transcribed chromatin and thus serves to specifically condense this euchromatic portion of chromosomes during the cell division cycle. ChIP-Seq data for Condensin II and Cohesin in v6.5 ESCs treated or not with the RNA polymerase II elongation inhibitor flavopiridol.

2012-02-09 | E-GEOD-30919 | biostudies-arrayexpress

Cohesin and CTCF Differentially Affect the Chromatin Architecture and Gene Expression in Human Cells

Project description:Recent studies of genome-wide chromatin interactions have revealed that the human genome is partitioned into many self-associating topological domains. The boundary sequences are enriched for binding sites of CTCF and the cohesin complex, implicating these two factors in the establishment or maintenance of topological domains. To determine the role of cohesin and CTCF in higher order chromatin architecture in human cells, we proteolytically cleaved the cohesin complex from interphase chromatin and examined changes in chromosomal organization as well as transcriptome. We observed a general loss of local chromosomal interactions upon disruption of cohesin complex, but the topological domains remain intact. However, we found that depletion of CTCF by RNA interference in these cells not only reduced intra-domain interactions but also increased inter-domain interactions. Further more, distinct groups of genes become mis-regulated upon depletion of cohesin and CTCF. Taken together, these observations suggest that CTCF and cohesin contribute in different ways to chromatin organization and gene regulation. Hi-C and mRNA-seq experiments in Cohesin and CTCF depleted HEK293 cells

2013-12-16 | E-GEOD-44267 | biostudies-arrayexpress

ChIP-Seq of Transcriptional Components in Colon carcinoma

Project description:Discovery of the genome-wide location of proteins using ChIP-Seq has allowed global mapping of the key transcription factors and chromatin regulators that control gene expression programs in various cells. Many DNA-associated processes are targeted for disease therapy. CDK8 is a kinase component of the Mediator co-activator complex and is often over-expressed in colorectal cancer. This study investigates the genome-wide localization of CDK8 in human colorectal cancer cells. Genomic DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. ChIP was performed using an antibody against H3K27ac and CDK8 as well as whole-cell extract (WCE) DNA controls.

2013-12-24 | E-GEOD-53602 | biostudies-arrayexpress

Histone profile for wild type MEF and secondary MEF with Dox-inducible vectors for Klf4, Sox2 and Oct4 (KSO)

Project description:Histone profile for wild type MEF and secondary MEF with Dox-inducible vectors for Klf4, Sox2 and Oct4 (KSO). ChIP-Seq data for H3K4me3, H3K27me3 and H3K9me3

2010-12-31 | E-GEOD-21271 | biostudies-arrayexpress

ChIP-Seq data for histone marks in mouse embryonic fibroblasts

Project description:The conversion of mouse embryonic fibroblasts (MEFs) to induced pluripotent stem cells (iPS) by forced expression of Oct4, Sox2 and Klf4 is among the earliest demonstrations of reprogramming to a pluripotent state by forced expression of transcription factors. To gain insights into the chromatin state of genes required for reprogramming, we profiled H3K4me3, H3K27me3 and H3K9me3. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. ChIP was performed using an antibody against H3K4me3, H3K27me3 and H3K9me3.

2011-01-19 | E-GEOD-26657 | biostudies-arrayexpress

Promoter proximal pausing and its regulation by c-Myc in embryonic stem cells: ChIP-Seq

Project description:Recruitment of the RNA Polymerase II (Pol II) transcription initiation apparatus to promoters by specific DNA binding transcription factors is well recognized as a key regulatory step in gene expression. We describe here evidence that promoter-proximal pausing is a general feature of transcription by Pol II in embryonic stem (ES) cells, and thus an additional step where regulation of gene expression may occur. We report here that c-Myc, which occupies a third of actively transcribed genes in ES cells and is a key regulator of cellular proliferation, binds P-TEFb and contributes to release of promoter-proximal paused Pol II at these genes. ChIP-seq data for Pol II and additional factors controlling pause release in mouse ES cells.

2010-04-02 | E-GEOD-20530 | biostudies-arrayexpress

Selective Inhibition of Tumor Oncogenes by Disruption of Super-Enhancers

Project description:Chromatin regulators have become highly attractive targets for cancer therapy, yet many of these regulators are expressed in a broad range of healthy cells and contribute generally to gene expression. An important conundrum has thus emerged: how can inhibition of a general regulator of gene expression produce selective effects at specific oncogenes? Here we investigate how inhibition of the transcriptional coactivator BRD4 (Bromodomain containing 4) leads to selective inhibition of disease-critical oncogenes in a highly malignant blood cancer, multiple myeloma (MM). We found that BRD4 generally occupies the promoter elements of active genes together with the Mediator coactivator, but remarkably high levels of these two coactivator proteins were associated with a small set of exceptionally large enhancers. These super-enhancers are associated with genes that feature prominently in MM biology, including the MYC oncogene. Treatment of MM tumor cells with the BET-bromodomain inhibitor JQ1 led to preferential loss of BRD4 at super-enhancers and consequent transcription elongation defects that preferentially impact genes with super-enhancers, including the c-MYC oncogene. Super-enhancers were found at key oncogenic drivers in many other tumor cells. Thus, super-enhancers can regulate oncogenic drivers in tumor cells, which in some cells can be preferentially disrupted by BRD4 inhibition, which in turn contributes to the selective transcriptional effects observed at these oncogenes. These observations have implications for the discovery of novel cancer therapeutics directed at components of super-enhancers in diverse tumor types. ChIP-Seq for chromatin regulators and RNA Polymerase II in multiple myeloma, glioblastoma multiforme, and small cell lung cancer

2013-01-02 | E-GEOD-42355 | biostudies-arrayexpress

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