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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE128327 | GEO | 2019/12/29

REPOSITORIES: GEO

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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

A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions [ChIP-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 | GSE131711 | GEO

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

2019-12-30 | GSE128326 | GEO

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

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 [RIP-seq]

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

| PRJNA526537 | 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

Requirement for SWI/SNF chromatin-remodeling complex in Tat-mediated activation of the HIV-1 promoter.

Project description:Activation of the human immunodeficiency virus type-1 (HIV-1) promoter in infected cells requires the sequential recruitment of several cellular factors to facilitate the formation of a processive elongation complex. The nucleosomal reorganization of the HIV-1 long terminal repeat (LTR) observed upon Tat stimulation suggests that chromatin-remodeling complexes could play a role during this process. Here, we reported that Tat interacts directly with Brm, a DNA-dependent ATPase subunit of the SWI/SNF chromatin-remodeling complex, to activate the HIV-1 LTR. Inhibition of Brm via small interfering RNAs impaired Tat-mediated transactivation of an integrated HIV-1 promoter. Furthermore, Brm is recruited in vivo to the HIV-1 LTR in a Tat-dependent manner. Interestingly, we found that Tat/Brm interaction is regulated by Tat lysine 50 acetylation. These data show the requirement of Tat-mediated recruitment of SWI/SNF chromatin-remodeling complex to HIV-1 promoter in the activation of the LTR.

| S-EPMC1440843 | biostudies-other

Human SWI/SNF directs sequence-specific chromatin changes on promoter polynucleosomes.

Project description:Studies in humans and other species have revealed that a surprisingly large fraction of nucleosomes adopt specific positions on promoters, and that these positions appear to be determined by nucleosome positioning DNA sequences (NPSs). Recent studies by our lab, using minicircles containing only one nucleosome, indicated that the human SWI/SNF complex (hSWI/SNF) prefers to relocate nucleosomes away from NPSs. We now make use of novel mapping techniques to examine the hSWI/SNF sequence preference for nucleosome movement in the context of polynucleosomal chromatin, where adjacent nucleosomes can limit movement and where hSWI/SNF forms altered dinucleosomal structures. Using two NPS templates (5S rDNA and 601) and two hSWI/SNF target promoter templates (c-myc and UGT1A1), we observed hSWI/SNF-driven depletion of normal mononucleosomes from almost all positions that were strongly favored by assembly. In some cases, these mononucleosomes were moved to hSWI/SNF-preferred sequences. In the majority of other cases, one repositioned mononucleosome appeared to combine with an unmoved mononucleosome forming a specifically localized altered or normal dinucleosome. These effects result in dramatic, template-specific changes in nucleosomal distribution. Taken together, these studies indicate hSWI/SNF is likely to activate or repress transcription of its target genes by generating promoter sequence-specific changes in chromatin configuration.

| S-EPMC2577362 | biostudies-other

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