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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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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

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

Mouse Smarcb1-deficient models recapitulate subtypes of human rhabdoid tumors.

Project description:Rhabdoid Tumors (RT) are highly aggressive tumors that are frequently localized in the central nervous system (CNS) where they are termed atypical teratoid and rhabdoid tumors (ATRT). We generated conditional Smarcb1-deficient mouse model leads to CNS Smarcb1-deficient tumors. We used microarrays to compared gene expression profilings of various human and mouse tumors. Our data demonstrate that the Smarcb1-deficient mouse model recapitulates the diversity of human RT.

2016-01-27 | GSE64019 | GEO

Gene expression analysis of human haploid cells (HAP1) depleted of SMARCB1 and SMARCA4

Project description:The aim of this study is to analyze the change in genome wide expression levels in HAP1 cells upon loss of SMARCB1, SMARCA4 or both these genes together. The SMARCB1 and SMARCA4 genes were the hits from a genome wide screen involving genetrap mutagenesis to find new players that are involved in sensitivity to Doxorubicin (Dox). It was found that loss of SMARCB1 and SMARCA4 genes impart resistance in HAP1 cells to Dox. To validate this, the genes were knocked out in HAP1 cells with CRISPR-Cas9 technology. Gene expression levels in SMARCB1 null, SMARCA4 null and SMARCB1-SMARCA4 double null cells were compared to wildtype HAP1 cells using RNAseq. From these experiments it was found that SMARCB1 loss caused several fold increase in ABCB1 gene levels. ABCB1 is an efflux pump in cells responsible for flushing out many small-molecule drugs. Further analysis of this gene confirmed that ABCB1 was the main factor responsible for Dox resistance upon SMARCB1 loss. In total there are four different cell types with two replicates for each cell type. Therefore, 8 samples in total.

2016-08-22 | E-GEOD-75515 | biostudies-arrayexpress

Tumor suppressor SMARCB1 suppresses super-enhancers to govern hESC lineage determination

Project description:The SWI/SNF complex is a critical regulator of pluripotency in human embryonic stem cells (hESCs), and individual subunits have varied and specific roles during development and in diseases. The core subunit SMARCB1 is required for early embryonic survival, and mutations can give rise to atypical teratoid/rhabdoid tumors (AT/RTs) in the pediatric central nervous system. We report that in contrast to other studied systems, SMARCB1 KD relieves bivalent gene repression in hESCs and promotes chromatin accessibility at super-enhancers. Moreover, and consistent with its established role as a CNS tumor suppressor, we find that SMARCB1 is essential for neural induction but dispensable for mesodermal or endodermal differentiation. Mechanistically, we demonstrate that SMARCB1 KD cells are robustly resistant to hESC super-enhancer silencing in neural differentiation conditions. This genomic assessment of hESC chromatin regulation by SMARCB1 reveals a novel positive regulatory function at super-enhancers and a unique lineage-specific role in regulating hESC differentiation.

2019-05-14 | GSE128351 | GEO

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

2013-12-31 | GSE46017 | GEO