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Regulation of DNA accessibility across the cell cycle by SWI/SNF complexes [ATAC-seq]

ABSTRACT: To identify dynamic changes in DNA accessibility with cell-cycle phase resolution following SWI/SNF inactivation, we compared the ATAC-seq signals in IMR32 cells treated with the small-molecule catalytic inhibitor of SWI/SNF BRM014 or DMSO, which were sorted by their cell cycle stage using a FUCCI live-cell fluorescent indicator. Analysis of these locations revealed that SWI/SNF-dependent sites are regulated in cyclic patterns throughout the cell cycle.

ORGANISM(S): Homo sapiens

PROVIDER: GSE205534 | GEO | 2023/10/24

REPOSITORIES: GEO

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DNA accessibility sites requiring SWI/SNF activity in AML [ATAC-seq]

Project description:To reveal the genome-wide targets of SWI/SNF complexes in AML cells, we performed ATAC-seq in THP-1, MOLM-13, and MV-4-11 cells with or without the SWI/SNF ATPase BRM014. Analysis of the locations decreased following 24 or 72 h after addition of BRM014 revealed that SWI/SNF-dependent sites are located at enhancers occupied by PU.1, especially the blood enhancer cluster (BENC), a set of enhancers that drives expression of MYC.

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Transcriptional changes in bone marrow cells upon SWI/SNF inhibition [scRNA-seq]

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Chromatin profiling following SWI/SNF inhibition in neuroblastoma cells [ChIP-seq]

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Genome-wide profile of the SWI/SNF chromatin remodeling complex

Project description:A systems understanding of nuclear organization and events is critical for determining how cells divide, differentiate and respond to stimuli and for identifying the causes of diseases. Chromatin remodeling complexes such as SWI/SNF have been implicated in a wide variety of cellular processes including gene expression, nuclear organization, centromere function and chromosomal stability, and mutations in SWI/SNF components have been linked to several types of cancer. To better understand the biological processes in which chromatin remodeling proteins participate we globally mapped binding regions for several components of the SWI/SNF complex throughout the human genome using ChIP-Seq. SWI/SNF components were found to lie near regulatory elements integral to transcription (e.g. 5M-bM-^@M-^Y ends, RNA Polymerases II and III and enhancers) as well as regions critical for chromosome organization (e.g. CTCF, lamins and DNA replication origins). To further elucidate the association of SWI/SNF subunits with each other as well as with other nuclear proteins we also analyzed SWI/SNF immunoprecipitated complexes by mass spectrometry. Individual SWI/SNF factors are associated with their own family members as well as with cellular constituents such as nuclear matrix proteins, key transcription factors and centromere components implying a ubiquitous role in gene regulation and nuclear function. We find an overrepresentation of both SWI/SNF-associated regions and proteins in cell cycle and chromosome organization. Taken together the results from our ChIP and immunoprecipitation experiments suggest that SWI/SNF facilitates gene regulation and genome function more broadly and through a greater diversity of interactions than previously appreciated. ChIP-Seq analysis of the SWI/SNF subunits Ini1, Brg1, BAF155 and BAF170 in HeLa S3 cells

2011-01-10 | E-GEOD-24397 | biostudies-arrayexpress

Changes of DNA accessibility and RNA transcription upon SWI/SNF inhibition in peripheral blood and bone marrow cells [multiome]

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siRNA Knockdown of SWI/SNF complex proteins in prostate cancer cell lines

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2024-06-05 | GSE242802 | GEO

Inhibition of SWI/SNF broadly disrupts enhancers and reveals remodeler redundancy at promoters

Project description:Appropriate gene expression requires the establishment of accessible chromatin at promoters and enhancers. These patterns are maintained thorugh the action of, such as the SWI/SNF family. Despite this critical role, previous studies have remained inconclusive regarding the direct role of SWI/SNF. Herein, we employ BRM014, a fast-acting small-molecule inhibitor of the SWI/SNF ATPase subunit, to probe the direct response of mouse embryonic stem cells to disruption of appropriate SWI/SNF chromatin remodeling activity. We demonstrate that the immediate role of SWI/SNF inhibition is a broad loss of chromatin accessibility at both promoter and enhancer loci, and this is reflected in an associated reduction in nascent transcription. We determine that this initial perturbation can be compensated for at a majority of gene promoters, such that these elements regain accessibilty and gene expression under prolonged treatment. However, a subset of gene promoters, as well as most enhancers, fail to recover under these conditions. Finally, we identify EP400 as a putative factor driving compensation ability, as the loss of this factor impedes promoter recovery.

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