Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Baf53a is involved in survival of mouse ES cells, which can be compensated by Baf53b.

ABSTRACT: The human Baf (Brg1/Brm associated factor) complex, also known as the mammalian SWI/SNF chromatin-remodeling complex, is involved in a variety of cellular processes. The pluripotency and self-renewal abilities are major characteristics of embryonic stem (ES) cells and are regulated by the ES cell-specific BAF (esBAF) complex. Baf53a is one of the subunits of the esBAF complex. Here, we found that growth of Baf53a-deficient ES cells was repressed, and expression of p53, p21, and cleaved Caspase 3 was increased. Interestingly, Baf53b, a homologue of Baf53a, rescued cell death of Baf53a-deficient ES cells. Baf53a-deficient ES cells overexpressing exogenous Baf53a or Baf53b remained in the undifferentiated state and proliferated. In summary, our findings suggest that Baf53a is involved in the survival of ES cells, and that Baf53b is able to compensate for this functional aspect of Baf53a.

ORGANISM(S): Mus musculus

PROVIDER: GSE103694 | GEO | 2017/11/16

SECONDARY ACCESSION(S): PRJNA404073

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

The study of dpf2 in mouse ES cells

Project description:Brg-or Brm-associated factor (BAF) complexes, is a 12 subunit complex which contains an ATPase subunit, Brg or Brm, that uses energy derived from ATP hydrolysis to disrupt histone:DNA contacts to catalyze transcriptional events such as promoting gene expression or repression. Genetic studies in mice demonstrated that BAF complexes are essential for early embryonic development and pluripotency. ES cells express distinctive compleses, termed esBAF complexes by the presence of BAF155, Brg, BAF60a. Purification of Brg and Brm-associated proteins reveals a new family of four stoichiometric subunits of mSWI/SNF or BAF complexes which was termed BAF45a, b, c, and d. The progenitors to both neurons and glia are maintained in a proliferative state by a specified SWI/SNF-like npBAF complex that contains both BAF45a and BAF53a. The transition from proliferative to neurogenic divisions requires the exchange of these subunites for the homologous BAF45b or BAF45c and BAF53b proteins. The function of BAF45d remwains unclear so far.At present, we found that the knockout of dpf2 in ES cells impared the differention of ES cells. We will identify the target genes of dpf2 by Chip-seq so that we could study how dpf2 affect the differentiation of ES cells into germ layers.Protocol: DNA was prepared from ES cells by standard ChIP method. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

2013-09-30 | E-ERAD-24 | biostudies-arrayexpress

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [CnR]

Project description:To determine whether the chromatin accessibility for YAP/TEADs in squamous cell carcinoma cells is directly regulated by BAF53A within BAF complexes, we performed CUT&RUN to profile the distribution of YAP, TEAD1, and BAF155 (a DNA binding subunit of BAF complexes) across the genome.

2021-10-29 | GSE156787 | GEO

TOP2 synergizes with BAF chromatin remodeling for resolution of facultative heterochromatin

Project description:Resolution and formation of facultative heterochromatin is essential to development, reprogramming, and oncogenesis. The mechanisms underlying these changes are poorly understood due to difficulty with interrogating heterochromatin dynamics and structure in vivo. BAF (mSWI/SNF) ATP-dependent chromatin remodeling complexes are known to promote chromatin accessibility. As the function of topoisomerase IIa (TOP2A) is largely dependent on BAF complexes in embryonic stem (ES) cells, we tested whether TOP2 was involved in BAF-mediated resolution of heterochromatin by performing ATAC-seq on ES cells treated with the TOP2 inhibitor ICRF-193, Brg1 (the primary ATPase subunit of esBAF complexes) conditional knockout cells, and Baf53a (a non-catalytic subunit dispensable for in vitro remodeling) conditional knockout cells. We found that TOP2 synergizes with BAF complexes genome-wide to resolve facultative heterochromatin to accessible chromatin at a large number of regulatory elements.

2017-03-01 | GSE94039 | GEO

BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex [RNA-seq]

Project description:mSWI/SNF or BAF chromatin regulatory complexes are dosage-sensitive regulators of human neural development frequently mutated in autism and intellectual disability. Cell cycle exit and differentiation of neural stem/progenitor cells is accompanied by BAF subunit switching to generate neuron-specific nBAF complexes. We manipulated the timing of BAF subunit exchange in vivo and found that early loss of the npBAF subunit BAF53a stalls cell cycle exit to disrupt neurogenesis. Loss of BAF53a results in decreased chromatin accessibility at specific neural transcription factor binding sites, including the pioneer factors Sox2 and Ascl1, due to Polycomb accumulation. This results in repression of cell cycle genes, thereby blocking cell cycle progression and differentiation. Cell cycle block upon Baf53a deletion could be rescued by premature expression of the nBAF subunit BAF53b but not by other major drivers of proliferation or differentiation. Wnt, EGF, FGF, Sox2, myc or Pax6 all fail to maintain proliferation in the absence of BAF53a, highlighting a novel mechanism underlying neural progenitor cell cycle exit in the continued presence of extrinsic proliferative cues.

2021-01-18 | GSE164990 | GEO

BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex [ATAC-seq]

2021-01-18 | GSE164989 | GEO

Expression data from Knockdown of BAF53A in DLD1 cell line

Project description:BAF53A, an important subunit of the SWI/SNF epigenetic chromatin regulatory complex, has been implicated as the driver of diverse cancers. However, the role of BAF53A in colorectal cancer (CRC) remains poorly understood.

2022-12-21 | GSE218008 | GEO

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [RNA-seq]

Project description:To identify genes regulated by BAF53A, we carried out RNA-seq analysis in three SCC cell lines after BAF53A knockdown by siRNA and in normal keratinocytes with BAF53A overexpression.

2021-10-29 | GSE156785 | GEO

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [ATAC-seq]

Project description:To identify accessible chromatin regions regulated BAF53A in squamous cell carcinomas (SCCs), we performed ATAC-seq in FaDu SCC cell lines after BAF53A knockdown by siRNA and in normal keratinocytes with BAF53A overexpression.

2021-10-29 | GSE156786 | GEO

A non-canonical BRD9-containing BAF chromatin remodeling complex regulates naïve pluripotency in mouse embryonic stem cells

Project description:The mammalian BRG1-associated factors (BAF) complex is a multi-subunit chromatin remodeling complex that is an important component of the embryonic stem cell (ESC) transcriptional regulatory network. However, the role of individual subunits in BAF complex targeting and function needs to be elucidated. Here, we find that the Bromodomain containing protein 9 (BRD9) defines a smaller, non-canonical BAF complex in mouse ESCs that is distinct from the canonical embryonic stem cell BAF (esBAF) and the polybromo-associated BAF (PBAF) complexes. This BRD9-containing BAF complex, or BBAF complex, uniquely incorporates the BRD4-interacting chromatin remodeling associated protein-like (BICRAL) or its paralog BICRA and lacks several esBAF subunits including BAF47, ARID1A and BAF57. We demonstrate that BBAF and esBAF complexes are targeted to different features of the genome and are co-bound with different sets of pluripotency transcription factors. Specifically, BBAF complexes co-localize with key regulators of naïve pluripotency, KLF4 and Sp5, on the genome. Consistent with this, we provide evidence that BBAF’s specific function is to regulate the transcription of genes involved in the maintenance of naïve pluripotency, including Nanog and Prdm14. Additionally, we show that BRD9 is displaced from chromatin by the selective BRD9 bromodomain inhibitor, I-BRD9, and that this leads to changes in target gene expression. Together, our results provide evidence for the identification of a new BAF complex, and demonstrate functionally specific roles for BAF complex assemblies in maintaining the transcriptional network of pluripotency.

2018-10-18 | PXD010670 | Pride

BAF250a regulates nucleosome occupancy and histone modification in priming embryonic stem cell differentiation

Project description:BAF complex is one major group of chromatin remodeling factors in mammals. However, how BAF regulated nucleosomes and other histone modifications is not clear. Here we delete BAF250a, a major component in esBAF to study the nucleosome and histone changes in ESCs. We find that deletion of BAF250a leads to nucleosome occupancy increase in TSS regions and non-pioneer transcription factor binding sites. BAF250a deletion also cause overall decrease of H3K27me3 modification. Collectively, these results reveals how BAF complex coordinates nucleosome, histone modification to control ESC function. Sample 1-4: Nucleosome profiles in WT and BAF250a KO ESCs. Sample 5-10: profiling of H3K4me3 and H3K27me3 in WT and BAF250 KO ESCs.

2015-08-03 | E-GEOD-59082 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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