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A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions [RIP-seq]

ABSTRACT: A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions [RIP-seq]

PROVIDER: PRJNA526537 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8710360.fastq.gz	Fastqsanger.gz
	SRR8710351.fastq.gz	Fastqsanger.gz
	SRR8710361.fastq.gz	Fastqsanger.gz
	SRR8710352.fastq.gz	Fastqsanger.gz
	SRR8710362.fastq.gz	Fastqsanger.gz

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A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions [RIP-seq]

2019-12-30 | GSE128139 | GEO

A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions [RNA-seq]

Project description:RNA is an essential component of the chromatin, influencing genome organization and expression. To investigate the role of lncRNAs in epigenetic activation, we profiled the RNA interactome of SWI/SNF complexes in proliferating and senescent conditions, when cells undergo widespread chromatin rearrangements. The isolation of transcripts associated to SMARCB1 core subunit, together with its chromatin binding profiling, showed prevalent association to active regions where it differentially binds ncRNAs locally transcribed. Among them, LINC00565 interacts with SMARCB1 exclusively in proliferating conditions, exerting a pro-oncogenic role in tumors with intact SWI/SNF complexes. LINC00565 is transcribed from an enhancer region and through binding to SMARCB1, controls the activation of GAS6 oncogene as part of a topologically organized region, as well the activation of a larger set of genes by favoring SMARCB1 binding. Our results indicate that LINC00565 influences the ability of the SWI/SNF complexes to drive epigenetic activation of specific promoters, suggesting a SWI/SNF-RNA cooperation to achieve transcriptional activation.

2019-12-30 | GSE128326 | GEO

A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions [ChIP-Seq]

2019-12-30 | GSE131711 | GEO

A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions

Project description:A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions

| PRJNA527128 | ENA

A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions [ChIP-Seq]

Project description:A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions [ChIP-Seq]

| PRJNA544487 | ENA

A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions [RNA-seq]

Project description:A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions [RNA-seq]

| PRJNA527129 | ENA

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

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.

2013-07-20 | E-GEOD-40384 | biostudies-arrayexpress

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

A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions.

Project description:LncRNAs have been shown to be direct players in chromatin regulation, but little is known about their role at active genomic loci. We investigate the role of lncRNAs in gene activation by profiling the RNA interactome of SMARCB1-containing SWI/SNF complexes in proliferating and senescent conditions. The isolation of SMARCB1-associated transcripts, together with chromatin profiling, shows prevalent association to active regions where SMARCB1 differentially binds locally transcribed RNAs. We identify SWINGN, a lncRNA interacting with SMARCB1 exclusively in proliferating conditions, exerting a pro-oncogenic role in some tumor types. SWINGN is transcribed from an enhancer and modulates the activation of GAS6 oncogene as part of a topologically organized region, as well as a larger network of pro-oncogenic genes by favoring SMARCB1 binding. Our results indicate that SWINGN influences the ability of the SWI/SNF complexes to drive epigenetic activation of specific promoters, suggesting a SWI/SNF-RNA cooperation to achieve optimal transcriptional activation.

| S-EPMC7028943 | biostudies-literature

ARID-DNA interactions are essential for SWI/SNF function

Project description:Every known SWI/SNF chromatin-remodeling complex incorporates an ARID DNA binding domain-containing subunit. Despite being a ubiquitous component of these complexes, physiological roles for this domain remain undefined. We screened an N-ethyl-N-nitrosurea (ENU) mutagenized library for ARID domain point mutations and generated an Arid1a/Baf250a hypomorphic allele. The mutant ARID1a (V1068G) protein is stably expressed at wild-type levels, and it is capable of assembling into a SWI/SNF complex with in vitro mononucleosome disruption activity. However, its capacity to bind DNA is lost. Consistent with defective DNA binding, mutant protein occupancy at known SWI/SNF target genes is decreased. Loss of DNA binding is associated with concurrent changes in SWI/SNF target gene expression. Mutant embryos manifest heart defects, fail to establish proper yolk sac vasculature, and exhibit hemorrhaging. As a result of these phenotypes, mutant embryos fail to establish proper circulation, culminating in ischemic arrest in utero between days 9.5 and 11.5. These data support a role for ARID1a-containing, BAF-A complexes in heart and extraembryonic vascular development, and indicate the ARID domain of ARID1a is essential in this regard. Hence, intrinsic ARID subunit-DNA interactions are required for normal SWI/SNF function in vivo. Four-condition experiment, wild-type vs Baf250a/Arid1a^V1068G/V1068G yolk sacs isolated at E8.5 and E9.5. Biological replicates: 3 per condition.

2012-01-15 | E-GEOD-32116 | biostudies-arrayexpress

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