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The mSWI/SNF ATPase module mediates subcomplex identity and non-catalytic targeting in SCCOHT [ChIP-seq]

ABSTRACT: The mSWI/SNF ATPase module mediates subcomplex identity and non-catalytic targeting in SCCOHT [ChIP-seq]

PROVIDER: PRJNA483038 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7608800.fastq.gz	Fastqsanger.gz
	SRR7608810.fastq.gz	Fastqsanger.gz
	SRR7608820.fastq.gz	Fastqsanger.gz
	SRR7608830.fastq.gz	Fastqsanger.gz
	SRR7608801.fastq.gz	Fastqsanger.gz

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The mSWI/SNF ATPase module mediates subcomplex identity and non-catalytic targeting in SCCOHT [ChIP-seq]

Project description:Perturbations to mammalian SWI/SNF (mSWI/SNF) chromatin remodeling complexes have been widely implicated as driving events across cancers1. One such perturbation is the dual loss of the SMARCA4 and SMARCA2 ATPase subunits, which has recently been implicated in rare cancers such as small cell carcinoma of the ovary, hypercalcemic type (SCCOHT)2-5, SMARCA4-deficient thoracic sarcomas6 and dedifferentiated endometrial carcinomas7. The consequences of SMARCA4/2 dual loss on the biochemical composition of the complex, chromatin targeting and remodeling capabilities, and subcomplex identity (BAF vs. PBAF) in these cancers are unknown. Here, we leverage SCCOHT cell lines to identify an unexpected ATPase module of mSWI/SNF subunits. Using biochemical and genome-wide profiling assays, we found that the incorporation of the ATPase module is a critical step in the functional specification of BAF and PBAF subcomplexes. Furthermore, by utilizing ATPase mutant variants, we found that the ATPase module mediates two separate and concurrent mSWI/SNF targeting mechanisms, evenly split between catalytically-independent targeting to primed enhancers/promoters and catalytically-dependent targeting to de novo enhancers. Finally, by linking these distinct sites to separate tumor-suppressive gene expression programs across ovarian tissues , we clarify the mechanistic consequences of SMARCA4/2 loss dual loss in these rare tumors.

2019-03-11 | GSE117734 | GEO

The mSWI/SNF ATPase module mediates subcomplex identity and non-catalytic targeting in SCCOHT [RNA-seq]

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The mSWI/SNF ATPase module mediates subcomplex identity and non-catalytic targeting in SCCOHT [ATAC-seq]

2019-03-11 | GSE117301 | GEO

The mSWI/SNF ATPase module mediates subcomplex identity and non-catalytic targeting in SCCOHT [ATAC-seq]

Project description:The mSWI/SNF ATPase module mediates subcomplex identity and non-catalytic targeting in SCCOHT [ATAC-seq]

| PRJNA481733 | ENA

The mSWI/SNF ATPase module mediates subcomplex identity and non-catalytic targeting in SCCOHT [RNA-seq]

Project description:The mSWI/SNF ATPase module mediates subcomplex identity and non-catalytic targeting in SCCOHT [RNA-seq]

| PRJNA481742 | ENA

The ATPase module of mammalian SWI/SNF family complexes mediates subcomplex identity and catalytic activity-independent genomic targeting

Project description:The ATPase module of mammalian SWI/SNF family complexes mediates subcomplex identity and catalytic activity-independent genomic targeting

| PRJNA483037 | ENA

Transcriptional profiling of 2 SCCOHT PDX models and the SCCOHT cell lines BIN67 and SCCOHT1

Project description:Transcriptional profiling of 2 SCCOHT patient-derived xenograft (PDX) models and 2 SCCOHT cell lines compared to normal ovary to investigate underlying biology of SCCOHT. RNA from 2 SCCOHT PDXs and 2 SCCOHT cell lines were individually hybridized with a pool of 2 commercial normal ovary RNA on Agilent whole human genome 4x44K microarrays.

2015-08-28 | E-GEOD-66434 | biostudies-arrayexpress

Transcriptional profiling of 2 SCCOHT PDX models and the SCCOHT cell lines BIN67 and SCCOHT1

Project description:Transcriptional profiling of 2 SCCOHT patient-derived xenograft (PDX) models and 2 SCCOHT cell lines compared to normal ovary to investigate underlying biology of SCCOHT.

2015-08-28 | GSE66434 | GEO

Identifying the genomic regions co-bound by ASCL1 and mSWI/SNF remodelers during neural differentiation [ChIP-seq]

Project description:We interfeered with the ASCL1-mSWI/SNF interaction: to abolish ASCL1 function, we knocked out ASCL1 in human iPSCs, while we used the BRM014 inhibitor to block the mSWI/SNF ATPase activity. We then performed ASCL1 ChIPseq in DIV24 WT and BRM014-treated neural cultures, and SMARCB1 ChIPseq in DIV24 WT and ASCL1 KO neural cultures, when ASCL1 expression is highest.

2023-03-14 | GSE214381 | GEO

Identifying the genomic regions where ASCL1 and mSWI/SNF remodelers are both required to regulate chromatin accessibility during neural differentiation [ATAC-seq]

Project description:We interfeered with the ASCL1-mSWI/SNF interaction: to abolish ASCL1 function, we knocked out ASCL1 in human iPSCs, while we used the BRM014 inhibitor to block the mSWI/SNF ATPase activity. We performed ATACseq in WT, ASCL1 KO, and BRM014-treated cells at DIV24, when ASCL1 expression is highest during neural differentiation.

2023-03-14 | GSE214380 | GEO

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