Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

EOMES safeguards TSC chromatin accessibility by directing BRG1 to TSC-associated loci [RNA-seq]

ABSTRACT: EOMES safeguards TSC chromatin accessibility by directing BRG1 to TSC-associated loci [RNA-seq]

PROVIDER: PRJNA1156180 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30534232_1.fastq.gz	Fastqsanger.gz
	SRR30534232_2.fastq.gz	Fastqsanger.gz
	SRR30534233_1.fastq.gz	Fastqsanger.gz
	SRR30534233_2.fastq.gz	Fastqsanger.gz
	SRR30534234_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 90

Similar Datasets

EOMES safeguards TSC chromatin accessibility by directing BRG1 to TSC-associated loci [RNA-seq]

Project description:EOMES is an essential transcription factor (TF) for murine trophoblast stem cell (TSC) maintenance. Despite that, the details of EOMES' function at the molecular level remain obscure. Here, we carried out rapid immunoprecipitation and mass spectrometry of endogenous protein (RIME) to identify TSC-specific protein interactors on EOMES. In addition to other established TFs involved in TSC maintenance, we found that EOMES interacts with several chromatin remodeller subunits, including BRG1. By exploiting an Eomes-degron system, we acutely depleted EOMES protein in TSCs and in parallel inhibited BRG1 function with small molecule BRM014. EOMES depletion and BRG1 inhibition resulted in reduced accessibility at largely overlapping genomic regions associated with TSC-related loci. Additionally, EOMES depletion results in misregulation of genes essential for TSC maintenance and function, as well as genes encoding cytoskeletal, cell-cell interaction and matricellular components.

2025-05-19 | GSE276261 | GEO

EOMES safeguards TSC chromatin accessibility by directing BRG1 to TSC-associated loci [CUT&RUN]

2025-05-19 | GSE276042 | GEO

EOMES safeguards TSC chromatin accessibility by directing BRG1 to TSC-associated loci [ATAC-seq]

2025-05-19 | GSE276039 | GEO

EOMES safeguards TSC chromatin accessibility by directing BRG1 to TSC-associated loci [ATAC-seq]

Project description:EOMES safeguards TSC chromatin accessibility by directing BRG1 to TSC-associated loci [ATAC-seq]

| PRJNA1154562 | ENA

EOMES safeguards TSC chromatin accessibility by directing BRG1 to TSC-associated loci [CUT&RUN]

Project description:EOMES safeguards TSC chromatin accessibility by directing BRG1 to TSC-associated loci [CUT&RUN]

| PRJNA1154558 | ENA

EOMES interacts with RUNX3 and BRG1 to promote innate memory cell formation through epigenetic reprogramming

Project description:Memory CD8+ T cells have the ability to provide lifelong immunity against pathogens. Although memory features generally arise after challenge with a foreign antigen, naïve CD8 single positive (SP) thymocytes may acquire phenotypic and functional characteristics of memory cells in response to cytokines such as interleukin-4. This process is associated with the induction of the T-box transcription factor Eomesodermin (EOMES). However, the underlying molecular mechanisms remain ill-defined. Using epigenomic profiling, we show that these innate memory CD8SP cells acquire only a portion of the active enhancer repertoire of conventional memory cells. This reprograming is secondary to EOMES recruitment, mostly to RUNX3-bound enhancers. Furthermore, EOMES is found within chromatin-associated complexes containing BRG1 and promotes the recruitment of this chromatin remodelling factor. Also, the in vivo acquisition of EOMES-dependent program is BRG1-dependent. In conclusion, our results support a strong epigenetic basis for the EOMES-driven establishment of CD8+ T cell innate memory program.

2019-06-06 | PXD014142 | Pride

Tbet-Eomes

Project description:Tbet-Eomes

| PRJNA706657 | ENA

Protein-protein interactions of BRG1 or BRG1-HSA in SW13 cells

Project description:The SWI/SNF complex remodels chromatin in an ATP-dependent manner through the ATPase subunits BRG1 and BRM. Chromatin remodeling alters nucleosome structure to change gene expression, however aberrant remodeling and gene expression can result in cancer. The function and localization on chromatin of the SWI/SNF complex depends on the protein makeup of the complex. Here we report the protein-protein interactions of wild-type BRG1 or mutant BRG1 in which the HSA domain has been deleted (BRG1-HSA). We demonstrate the interaction of BRG1 with most SWI/SNF complex members and a failure of a number of these members to interact with BRG1-HSA. These results demonstrate that the HSA domain of BRG1 is a critical interaction platform for the correct formation of SWI/SNF remodeling complexes.

2023-02-15 | PXD029647 | Pride

Chromatin remodeler Brahma safeguards labile canalization of cardiac mesoderm differentiation

Project description:Differentiation proceeds along a continuum of increasingly fate-restricted intermediates, referred to as canalization. Canalization is essential for stabilizing cell fate, but mechanisms underlying robust canalization are unclear. Here we show that the BRG1/BRM-associated factor (BAF) chromatin remodeling complex ATPase gene Brm safeguards cell identity during directed cardiogenesis of mouse embryonic stem cells. Despite establishment of well-differentiated precardiac mesoderm, Brm-null cells predominantly became neural precursors, violating germ layer assignment. Trajectory inference showed sudden acquisition of non-mesodermal identity in Brm-null cells, consistent with a new transition state referred to as a saddle-node bifurcation. Mechanistically, loss of Brm prevented de novo accessibility of cardiac enhancers while increasing expression of neurogenic factor POU3F1, preventing expression of neural suppressor REST, and disrupting composition of BRG1 complexes. Brm mutant identity switch was overcome by increasing BMP4 levels during mesoderm induction. Mathematical modeling supports all our observations. In the mouse embryo, Brm deletion exacerbated mesoderm-deleted Brg1 mutant phenotypes, severely compromising cardiogenesis, unmasking an in vivo role for Brm. Our results reveal Brm as a compensable safeguard of the fidelity of mesoderm chromatin states, and support a model in which developmental canalization is not a rigid irreversible path, but a highly plastic trajectory.

2021-11-03 | PXD026638 | Pride

Gene expression of sorted Eomes+ and Eomes‒ γδ T cells from spleen of Eomes-IRES-GFP mice.

Project description:Eomesodermin (Eomes) is a transcription factor with a crucial role regulating cytotoxic function, development and survival of immune cells. Although it is known that γδ T cells can express Eomes, its function on those cells is still largely unknown. Using Eomes-IRES-GFP mice we were able to sort for Eomes+ and Eomes‒ γδ T cells populations and get their gene expression profiles, bringing light to the role of Eomes on γδ T cells.

2017-04-10 | GSE85585 | 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