Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide maps of histone PTMs and co-factors in pluripotent mouse embryonic stem cells (mESCs) and epiblast-like cells (EpiLCs)

ABSTRACT: We report here the genome wide mapping of histone PTMs and chromatin bound factors in pluripotent control and H3K27R base edited mouse embryonic stem cells (mESCs) and epiblast-like cells (EpiLCs) using ChIP-Seq technology. We have deposited results from chromatin immunoprecipitations done using antibodies against Rpb1 (Pol-II), Med1,H3.3, H3K27me1, H3K27me2, H3K27me3 and H3K27ac (rabbit and mouse monoclonal antibodies). We show the loss of all H3K27 from H3.1/2/3 results in loss of associated K27 methylation and acetylation as expected. In such cells, there are only modest changes to MED1 or RNA Pol-II binding or activity that correlate with transcriptional status, suggesting that H3K27ac is not required to initiate or maintain transcription of genes, while loss of H3K27me3 associates with derepression of Polycomb target genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE160974 | GEO | 2021/12/06

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Disruption of cardiac Med1 inhibits RNA polymerase-II promoter occupancy and induces chromatin remodeling

Project description:The Mediator co-activator complex directs gene specific expression by binding distal enhancer-bound transcription factors through its Med1 subunit while bridging to RNA Polymerase-II (Pol-II) at gene promoters. In addition, Mediator scaffolds epigenetic modifying enzymes that determine local DNA accessibility. We previously found that deletion of Med1 in cardiomyocytes deregulates more than 5000 genes and promotes acute heart failure and hypothesize Med1 deficiency disrupts enhancer-promoter coupling. Using ChIP-seq, we find Pol-II pausing index is increased in Med1 knockout versus floxed control hearts primarily from decreased Pol-II occupancy at the majority of transcriptional start sites. Med1-dependent gene expression correlates strongly with histone H3 K27 acetylation while H3 K27 tri-methylated levels are increased and inversely correlate with absolute expression levels. Furthermore, Med1 deletion leads to dynamic changes in acetyl-K27 associated super-enhancer regions and their enriched transcription factor binding motifs that are consistent with altered gene expression. Our findings suggest that Med1 is important in establishing enhancer-promoter coupling in the heart by facilitating the recruitment of Pol-II to gene promoters, determining chromatin accessibility within genes and enhancer regions and altering transcription factor binding motifs that are likely important in directing gene-specific expression.

2019-10-30 | GSE118965 | GEO

CUT&Tag_STARR-seq of OE19 cell line

Project description:To investigate enhancer activity in OE19 cells, we performed CUT&Tag_STARR-seq using antibodies against H3K27ac, BRD4 and MED1 .

2024-09-25 | E-MTAB-14155 | biostudies-arrayexpress

ATAC_STARR-seq and CUT&Tag_STARR-seq of OE19 cell line

Project description:To investigate enhancer activity in OE19 cells, we performed ATAC_STARR-seq and CUT&Tag_STARR-seq using antibodies against H3K27ac, BRD4 and MED1 .

2024-09-24 | E-MTAB-14083 | biostudies-arrayexpress

Histone H3.3 lysine 9 and 27 control repressive chromatin states at cryptic cis-regulatory elements and bivalent promoters in mouse embryonic stem cells

Project description:Histone modifications are associated with distinct transcriptional states, but it is unclear whether they instruct gene expression. To investigate this, we mutated histone H3.3 K9 and K27 residues in mouse embryonic stem cells (mESCs). Here, we find that H3.3K9 is essential for controlling specific distal intergenic regions and for proper H3K27me3 deposition at promoters. The H3.3K9A mutation resulted in decreased H3K9me3 at regions encompassing endogenous retroviruses and induced a gain of H3K27ac and nascent transcription. These changes in the chromatin environment unleashed cryptic enhancers, resulting in the activation of distinctive transcriptional programs and culminating in protein expression normally restricted to specialized immune cell types. The H3.3K27A mutant disrupted deposition and spreading of the repressive H3K27me3 mark, particularly impacting bivalent genes with higher basal level of H3.3 at promoters. Therefore, H3.3K9 and K27 crucially orchestrate repressive chromatin states at cis-regulatory elements and bivalent promoters, respectively, and instruct proper transcription in mESCs.

2024-06-24 | MSV000095134 | MassIVE

EGAS00001003953-ChIPseq - samples

Project description:ChIPseq data for human glioblastoma patients, EGAS00001003953. Mix of input, H3K27ac, H3K27me1, H3K27me3, H3K36me3, H3K4me1, H3K4me3, H3K9me3 and BRD, 20 human samples, 2 cell lines (LN229, ZH487).

| EGAD00001006548 | EGA

Genome-wide map of 4 histone modifications and PolII in iPSC-derived human cardiomyocytes

Project description:We generated maps of H3K4me1, H3K27ac (enhancers), H3K4me3, Pol II (promoters) and H3K27me3 (repressed chromatin) in the genome of human iPSC-derived cardiomyocytes Differentiation of cardiomyocytes from iPSC followed by ChIP-seq of H3K27ac, H34me1, H327me3, H3K4me3 and PolII

2016-02-22 | E-GEOD-77267 | biostudies-arrayexpress

ChIP-seq analysis of BRD4, MED1 and P65 in SCC1 cells after JQ1 treatment

Project description:To explore genome-wide alteration of BRD4, MED1, p65 and H3K27Ac during BET inhibition, we performed chromatin immunoprecipitation sequencing (ChIP-seq) of SCC1 cells to examine genome-wide recruitment of the MED1, BRD4, p65 and H3K27ac following JQ1 treatment. BET inhibition by JQ1 led to dramatically loss of the recruitment of MED1, BRD4 and p65 at a cohort of key oncogenes associate with tumorigenesis and metastasis. Suggesting BET inhibition is effective strategy to suppress the tumorigenesis and metastasis of head and neck squamous cell carcinoma.

2021-05-05 | GSE131710 | GEO

Establishment of a novel in vitro transcription assay

Project description:RNA Polymerase II (Pol II) transcriptional recycling is an underappreciated mechanism for which the required factors and contributions to overall gene expression levels are poorly understood. We describe an in vitro methodology facilitating unbiased identification of putative RNA Pol II transcriptional recycling factors and quantitative measurement of transcriptional output from recycled transcriptional components. By combing our in vitro transcription assays with other experiments (e.g. in vivo dynamic ChIP-seq assays), we identified PAF1 complex components and phospho-MED1 as drivers for transcription recycling, revealing a new layer in controlling Pol II-dependent transcription. Our findings also point to RNA Pol II transcription recycling as a mechanism that functions aberrantly in disease states such as cancer, and indicate the potential to target factors such as PAF1 and phospho-MED1 that drive RNA Pol II recycling in cancer.

2021-11-03 | PXD017881 | Pride

Chromatin occupancy of key transcriptional regulators in the presence of the BET bromodomain inhibitor JQ1

Project description:MM1.S cells are an aggressive dexamethasone sensitive multiple myeloma cell line whose transcritional program is driven by deregulated c-Myc activity. We present ChIP-seq analysis of key transcritional regulators that are implicated the c-Myc transcriptional network in MM1.S cells treated with vehicle or 500nM JQ1. Brd4, Cdk9, cMyc, Max, Med1, RNA Pol II, and the chromatin modifications H3K4me3 and H3K27Ac were profiled in MM1.S cells treated with 500nM JQ1 for 24hr

2012-11-30 | E-GEOD-42161 | biostudies-arrayexpress

The Mediator Kinase Complex Cooperates with Swi/Snf to Regulate Lineage-Resolved Enhancers and Differentiation [ChIP-Seq]

Project description:Depletion of CDK8 and its paralogue CDK19 in intestinal organoids resulted in the downregulation of genes associated with intestinal secretory cells. To determine the consequence of loss of CDK8/19 in re-defining enhancers we performed ChIP sequencing for MED1, MED12, H3K27Ac and ARID1A. We identified that loss of MED1 and MED12 at super enhancers regulating key intestinal transcription factors and loss of ARID1A binding across intestinal (super-)enhancers.

2022-10-19 | GSE191121 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data