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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE190721 | GEO | 2023/01/10

REPOSITORIES: GEO

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Transcriptional effects of SWI/SNF inhibition in acute myeloid leukemia cells [RNA-seq]

Project description:To reveal the effects of SWI/SNF inhibition in KMT2Ar leukemic cells, we performed RNA-seq in THP-1, MOLM-13, and MV-4-11 cells, and compared the effects of BRM014 with DMSO vehicle control. We also compared these effects to PMA-induced differentiation in THP-1 cells, as well as treatment with the PU.1 inhibitor DB2313. Analysis of transcripts reveal that SMARCA4 inhibition promotes differentiation, down-regulation of MYC and its target genes, and reduced expression of CD44, consistent with loss of self-renewal.

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Chromatin occupancy profiling of AML transcription factors upon SWI/SNF inhibition [ChIP-seq]

Project description:To reveal the effects of SWI/SNF inhibition on genome-wide transcription factor occupancy in AML cells, we performed ChIP-seq in THP-1 cells, and compared the effects of BRM014 with DMSO vehicle control. We also examined the effects of SMARCA4 chromatin targeting via treatment with the PU.1 inhibitor DB2313. Analysis of genome-wide occupancy by ChIP-seq reveals that SWI/SNF inhibition impairs PU.1-directed enhancer programs in AML cells.

2023-01-10 | GSE217171 | GEO

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

Project description:Despite significant therapeutic potential of SWI/SNF inhibition therapy, the off-tumor effects of SWI/SNF inhibition remain largely unknown. Here, we quantify the effects of the dual SWI/SNF ATPase inhibitor BRM014 on bone marrow cells in mice. We identify lineage-dependent effects on the B and monocyte lineages within the bone marrow.

2023-01-10 | GSE205571 | 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.

2023-11-02 | GSE198517 | GEO

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

Project description:To assess the genome-wide effects of SWI/SNF activity in MYCN-amplified neuroblastoma cells, we performed ChIP-seq in IMR-32 cells treated with either DMSO or the SWI/SNF inhibitor BRM014. Pronounced loss of chromatin occupancy was observed for members of the neuroblastoma core regulatory circuitry within 1 hour.

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

Project description:Despite significant therapeutic potential of SWI/SNF inhibition therapy, the off-tumor effects of SWI/SNF inhibition remain largely unknown. Here, we quantify the effects of the dual SWI/SNF ATPase inhibitor BRM014 on peripheral blood (PB) and bone marrow (BM) cells in mice. We identify altered chromatin regulatory mechanisms in B cells and monocytes.

2023-01-10 | GSE205570 | GEO

DNA accessibility sites requiring SMARCA4 activity in neuroblastoma cells [ATAC-seq]

Project description:To reveal the genome-wide targets of SWI/SNF complexes in neuroblastoma cells, we performed ATAC-seq in IMR-32 cells with or without SMARCA4 inactivation. To identify changes in DNA accessibility following SMARCA4 inactivation, we used either the small-molecule catalytic inhibitor BRM014, auxin-induced degradation of IMR-32 cells engineered with SMARCA4 tagged to the minimal auxin-induced degron (SMARCA4-mAID), or the corresponding vehicle controls. Analysis of these locations reveal that SMARCA4-dependent sites are located at enhancers used by the neuroblastoma core regulatory circuitry.

2023-10-24 | GSE190706 | GEO

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

Project description: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.

2023-10-24 | GSE205534 | GEO

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

The SWI/SNF chromatin remodeling complex is required for lineage specific enhancer activity [MEF_ChIP]

Project description:Genes encoding subunits of SWI/SNF (BAF) chromatin remodeling complexes are collectively altered in over 20% of all human malignancies, but the mechanisms by which these complexes alter chromatin to modulate transcription and control cell fate are poorly understood. Utilizing both loss-of-function and gain-of-function approaches, here we show that SWI/SNF complexes are preferentially targeted to distal enhancers and interact with p300 to regulate transcription via modulation of histone H3 lysine 27 acetylation. We identify a greater requirement for SWI/SNF at typical enhancers than at most super-enhancers and at enhancers in untranscribed regions than in transcribed regions. Our data further demonstrate that SWI/SNF-dependent distal enhancers are essential for controlling expression of genes linked to developmental processes. Our findings thus establish SWI/SNF complexes as regulators of the enhancer landscape and provide insight into the roles of SWI/SNF in cellular fate control.

2016-11-21 | GSE71507 | GEO

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