DNA accessibility sites requiring SWI/SNF activity in AML [ATAC-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA788271 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17208757_1.fastq.gz | Fastqsanger.gz | |||
| SRR17208757_2.fastq.gz | Fastqsanger.gz | |||
| SRR17208758_1.fastq.gz | Fastqsanger.gz | |||
| SRR17208758_2.fastq.gz | Fastqsanger.gz | |||
| SRR17208759_1.fastq.gz | Fastqsanger.gz |
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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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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.
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Project description:Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus siRNAs targeting SWI/SNF complex proteins (SMARCA2, SMARCA4, and SMARCB1). Goal was to determine the effect of SWI/SNF knockdown on gene expression in prostate cancer. Two-condition experiment: non-targeting siRNA versus SWI/SNF-siRNA treated cells. Three SWI/SNF proteins were targeted: SMARCA2, SMARCA4, and SMARB1. Biological replicates: 1 control replicate, 2 treatment replicates per SWI/SNF protein. Technical replicates: 1 replicate per SWI/SNF protein. Cell lines: 22Rv1 and LNCaP.
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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
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Project description:This study profiles chromatin accessibility, gene expresison, transcription factor binding, and three-dimensional DNA-DNA contact changes upon rapid SWI/SNF ATPase inactivation in prostate cancer cells. SWI/SNF ATPases activity was disabled using a novel PROTAC degrader compound targeting the SMARCA2, SMARCA4 and PBRM1 subunits of the SWI/SNF remodeling complex.
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Project description:This study profiles chromatin accessibility, gene expresison, transcription factor binding, and three-dimensional DNA-DNA contact changes upon rapid SWI/SNF ATPase inactivation in prostate cancer cells. SWI/SNF ATPases activity was disabled using a novel PROTAC degrader compound targeting the SMARCA2, SMARCA4 and PBRM1 subunits of the SWI/SNF remodeling complex.
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