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Smarcb1 is indispensable for the nervous system development and its loss results in a deregulation of esBAF binding.

ABSTRACT: Smarcb1 is indispensable for the nervous system development and its loss results in a deregulation of esBAF binding.

PROVIDER: PRJNA775001 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16596713.fastq.gz	Fastqsanger.gz
	SRR16596714.fastq.gz	Fastqsanger.gz
	SRR16596715.fastq.gz	Fastqsanger.gz
	SRR16596716.fastq.gz	Fastqsanger.gz
	SRR16596717.fastq.gz	Fastqsanger.gz

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Similar Datasets

Smarcb1 is indispensable for the nervous system development and its loss results in a deregulation of esBAF binding [ChIP-seq]

Project description:Using ChIP-seq technology, we aimed to provide insight into the consequences of the knockdown of Smarcb1, an essential esBAF subunit, for the binding of the esBAF complex (Smarca4), the PRC2 complex (Ezh2) as well as for histone marks H3K27me3, H3K27ac and H3K4me3. We show that Smarcb1 knockdown results in the change of BAF complex binding in both directions: decreased binding (potentially by loss of function) as well as increased binding (potentially by retargeting). Furthermore, we see that binding changes especially occur in regions important for basic cellular functions (adhesion, cell organization, metabolism) as well as regions crucial for development (especially nervous system development). In addition, we depicted binding changes in enhancer regions in which a decrease of BAF binding was much more prominent than in gene regions.

2022-04-27 | GSE186667 | GEO

Smarcb1 is indispensable for the nervous system development and its loss results in a deregulation of esBAF binding [RNA-seq]

Project description:Using RNA-seq technology, we aimed to provide insight into the consequences of the knockdown of Smarcb1, an essential esBAF subunit, for the gene expression of murine embryonic stem cells. We were able to show that knockdown cells show both, an upregulation and a downregulation, of a high number of genes. Further, many of these genes are connected to central cellular processes like cell organization or cell adhesion as well as to critical developmental processes like nervous system development.

2022-04-27 | GSE186668 | GEO

Smarcb1 is indispensable for the nervous system development and its loss results in a deregulation of esBAF binding [RNA-seq]

Project description:Smarcb1 is indispensable for the nervous system development and its loss results in a deregulation of esBAF binding [RNA-seq]

| PRJNA775007 | ENA

Smarcb1 is indispensable for the nervous system development and its loss results in a deregulation of esBAF binding [ChIP-seq]

Project description:Smarcb1 is indispensable for the nervous system development and its loss results in a deregulation of esBAF binding [ChIP-seq]

| PRJNA775008 | ENA

Smarcb1 is indispensable for the nervous system development and its loss results in a deregulation of esBAF binding.

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-04-27 | GSE186669 | GEO

Smarcb1 Loss Results in a Deregulation of esBAF Binding and Impacts the Expression of Neurodevelopmental Genes.

Project description:The murine esBAF complex plays a major role in the regulation of gene expression during stem cell development and differentiation. As one of its core subunits, Smarcb1 is indispensable for its function and its loss is connected to neurodevelopmental disorders and participates in the carcinogenesis of entities such as rhabdoid tumours. We explored how Smarcb1 regulates gene programs in murine embryonic stem cells (mESC) and in this way orchestrates differentiation. Our data underline the importance of Smarcb1 expression and function for the development of the nervous system along with basic cellular functions, such as cell adhesion and cell organisation. Using ChIP-seq, we were able to portray the consequences of Smarcb1 knockdown (kd) for the binding of esBAF and PRC2 as well as its influence on histone marks H3K27me3, H3K4me3 and H3K27ac. Their signals are changed in gene and enhancer regions of genes connected to nervous system development and offers a plausible explanation for changes in gene expression. Further, we describe a group of genes that are, despite increased BAF binding, suppressed after Smarcb1 kd by mechanisms independent of PRC2 function.

| S-EPMC9027123 | biostudies-literature

esBAF is an essential component of the core pluripotency transcriptional network

Project description:Distinctive SWI/SNF-like ATP-dependent chromatin remodeling esBAF complexes are indispensable for the maintenance and pluripotency of mouse embryonic stem (ES) cells. To understand the mechanism underlying the roles of these complexes in ES cells, we performed high-resolution genome-wide mapping of the core ATPase subunit, Brg, using ChIP-Seq technology. We find that that esBAF, as represented by Brg, binds to genes encoding components of the core ES transcriptional circuitry, including Polycomb group proteins. esBAF colocalizes extensively with Oct4, Sox2 and Nanog genome-wide, and shows distinct functional interactions with Oct4 and Sox2 at its target genes. Surprisingly, no significant colocalization of esBAF with PRC2 complexes, represented by Suz12, is observed. Lastly, esBAF co-binds with Stat3 and Smad1 genome-wide, consistent with a direct and critical role in LIF and BMP signaling essential to maintain pluripotency. Taken together, our studies indicate that esBAF is both an essential component of the core pluripotency transcriptional network, and might also be a critical component of the LIF and BMP signaling pathways essential for maintenance of self-renewal and pluripotency. Brg knockdown effect on expression, Brg ChIP-Seq

2009-01-20 | E-GEOD-14344 | biostudies-arrayexpress

esBAF is an essential component of the core pluripotency transcriptional network

2009-01-20 | GSE14344 | GEO

Transcriptional response to Smarcb1 re-expression in murine derived Smarcb1 deficient p53 null tumors

Project description:SMARCB1 (Snf5/Ini1/Baf47) is a potent tumor suppressor, the loss of which serves as the diagnostic feature in Malignant Rhabdoid Tumors (MRT) and Atypical Teratoid/Rhabdoid Tumors (AT/RT), two highly aggressive forms of pediatric neoplasms. Here, we restore Smarcb1 expression in cells derived from Smarcb1-deficient tumors which developed in Smarcb1-heterozygous p53-/- mice. Profiling Smarcb1 dependent gene expression we find genes which are dependent on Smarcb1 expression to be enriched for ECM and cell adhesion functions. We identify Igfbp7, which is related to the insulin-like growth factor binding proteins family, as a downstream target of Smarcb1 transcriptional activity, and show that re-introduction of Igfbp7 alone can hinder tumor development. Two cancer cell lines, 167 and 365, derived from Smarcb1-deficient tumors which developed in Smarcb1-heterozygous p53-/- mice were re-infected with a retro-viral vector for Smarcb1 re-expression or an empty retro-viral vector as control. Total-RNA was collected 3 days post infection so as to enrich for direct targets of Smarcb1 transcriptionaly regulated genes

2013-12-31 | E-GEOD-46017 | biostudies-arrayexpress

Suppression of pervasive noncoding transcription in embryonic stem cells by esBAF

Project description:Approximately 75% of the human genome is transcribed, the majority of which does not encode protein. However, most noncoding RNA (ncRNA) is rapidly degraded after transcription, and relatively few have established functions, questioning the significance of this observation. Here we show that esBAF, a SWI/SNF family nucleosome remodeling factor, suppresses transcription of ncRNAs from approximately 57,000 nucleosome-depleted regions (NDRs) throughout the genome of mouse embryonic stem cells (ESCs). We show that esBAF functions both to keep NDRs nucleosome-free and to promote elevated nucleosome occupancy adjacent to NDRs. Reduction of adjacent nucleosome occupancy upon esBAF depletion is strongly correlated with ncRNA expression, suggesting that flanking nucleosomes form a barrier to pervasive transcription. Upon forcing nucleosome occupancy near an NDR using a nucleosome-positioning sequence, we find that esBAF is no longer required to silence transcription. These data reveal a novel role for esBAF in suppressing pervasive transcription from open chromatin regions in ESCs.

2015-02-12 | GSE57170 | GEO

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