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MSWI/SNF promotes polycomb repression both directly and through genome-wide redistribution [RNA-seq]

ABSTRACT: mSWI/SNF promotes polycomb repression both directly and through genome-wide redistribution [RNA-seq]

PROVIDER: PRJNA725842 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14344128.fastq.gz	Fastqsanger.gz
	SRR14344129.fastq.gz	Fastqsanger.gz
	SRR14344130_1.fastq.gz	Fastqsanger.gz
	SRR14344130_2.fastq.gz	Fastqsanger.gz
	SRR14344131_1.fastq.gz	Fastqsanger.gz

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mSWI/SNF promotes polycomb repression both directly and through genome-wide redistribution [ChIP-seq]

Project description:mSWI/SNF promotes polycomb repression both directly and through genome-wide redistribution [ChIP-seq]

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mSWI/SNF promotes Polycomb repression both directly and through genome-wide redistribution.

Project description:The mammalian SWI/SNF complex, or BAF complex, has a conserved and direct role in antagonizing Polycomb-mediated repression. Yet, BAF also promotes repression by Polycomb in stem cells and cancer. How BAF both antagonizes and promotes Polycomb-mediated repression remains unknown. Here, we utilize targeted protein degradation to dissect the BAF-Polycomb axis in mouse embryonic stem cells on short timescales. We report that rapid BAF depletion redistributes Polycomb repressive complexes PRC1 and PRC2 from highly occupied domains, like Hox clusters, to weakly occupied sites normally opposed by BAF. Polycomb redistribution from highly repressed domains results in their decompaction, gain of active epigenomic features and transcriptional derepression. Surprisingly, through dose-dependent degradation of PRC1 and PRC2, we identify a conventional role for BAF in Polycomb-mediated repression, in addition to global Polycomb redistribution. These findings provide new mechanistic insight into the highly dynamic state of the Polycomb-Trithorax axis.

| S-EPMC8504423 | biostudies-literature

mSWI/SNF promotes polycomb repression both directly and through genome-wide redistribution [ChIP-seq]

Project description:The mammalian SWI/SNF, or BAF complex, has a conserved and direct role in antagonizing polycomb-mediated repression. Yet, BAF also promotes repression by polycomb in stem cells and cancer. How BAF both antagonizes and promotes polycomb-mediated repression remains unknown. Here, we utilize targeted protein degradation to dissect the BAF-polycomb axis in embryonic stem cells on short timescales. We report that rapid BAF depletion redistributes PRC1 and PRC2 complexes from highly occupied domains, like Hox clusters, to weakly occupied sites normally opposed by BAF. Polycomb redistribution from highly repressed domains results in their decompaction, gain of active epigenomic features, and transcriptional derepression. Surprisingly, through dose-dependent degradation of PRC1 & PRC2 we identify a conventional role for BAF in polycomb-mediated repression, in addition to global polycomb redistribution. These findings provide new mechanistic insight into the highly dynamic state of the Polycomb-Trithorax axis.

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mSWI/SNF promotes polycomb repression both directly and through genome-wide redistribution [RNA-seq]

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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.

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mSWI/SNF promotes distal repression by titrating polycomb dosage

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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.

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mSWI/SNF functional genomic characterization of SMARCB1 mutants in SMARCB1-null and heterozygous settings

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Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [ATAC-seq]

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