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Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [RNA-Seq]

ABSTRACT: Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [RNA-Seq]

PROVIDER: PRJNA1146038 | ENA |

REPOSITORIES: ENA

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Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation

Project description:Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation

| PRJNA1146458 | ENA

Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [CUT&Run]

Project description:ATP-dependent chromatin remodelers establish and arrange nucleosome distribution, modifying accessibility of DNA. Brg1 is exclusive ATPase subunit of mSWI/SNF complex. To understand the dosage dependent function of mSWI/SNF complex. We take an advantage of dTag system to precisely control abundancy of BRG1. We found overall Brg1-binding is sensitive to its abundance nevertheless OCT4-target or H3K27ac region, suggesting Brg1 genome-wide distribution rather than being actively recruited. We also reveal open chromatin dependency on BRG1. The chromatin accessibility of super enhancer shows buffered response on depletion of BRG1, whereas weak enhancer is sensitive. Finally, transcriptomic analysis identified that transcription shows buffered dependencies on BRG1 loss. Overall, our results highlight kinetics differences of BRG1-binding to transcriptome underline BRG1 dosage-sensitive mechanism.

2025-01-01 | GSE274358 | GEO

Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [ATAC-Seq]

2025-01-01 | GSE274357 | GEO

Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [RNA-Seq]

2025-01-01 | GSE274356 | GEO

Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [ATAC-Seq]

Project description:Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [ATAC-Seq]

| PRJNA1146037 | ENA

Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [CUT&Run]

Project description:Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [CUT&Run]

| PRJNA1146040 | ENA

mSWI/SNF promotes distal repression by titrating polycomb dosage

Project description:mSWI/SNF promotes distal repression by titrating polycomb dosage

| PRJNA605717 | ENA

Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation

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

2025-01-01 | GSE274469 | 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

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

Project description:Chromatin remodeling complexes regulate gene expression by shifting, evicting, and exchanging nucleosomes along the chromosomes of eukaryotic organisms. The mammalian SWI/SNF chromatin remodeling complex (mSWI/SNF or BAF) is mutated in over 20% of human cancers and loss of the SMARCB1 gene, encoding the BAF47 protein subunit, results in one of the most aggressive and lethal pediatric cancers. An accumulation of point mutations occurs at the C-terminal end of the protein, for which the functional ramifications are unknown. We previously demonstrated that reintroduction of SMARCB1 in SMARCB1-null malignant rhabdoid tumor cells results in a genome-wide increase of mSWI/SNF complex occupancy coupled with activation of PRC2-repressed genes. Here, we study the functional consequences that these point mutations exert on mSWI/SNF complex activity in SMARCB1-deficient tumor cells and extend this investigation to a CRISPR/Cas9-mediated SMARCB1-heterozygous mutant induced pluripotent stem cell. Intriguingly, we observe that the mutant complexes bind similarly to wild-type SMARCB1 complexes at enhancers throughout the genome but often fail to transcriptionally activate nearby genes in a cis-regulatory manner.

2019-11-21 | GSE124903 | GEO

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