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Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription [HiC-Seq]

ABSTRACT: Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription [HiC-Seq]

PROVIDER: PRJNA491667 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7868823_1.fastq.gz	Fastqsanger.gz
	SRR7868823_2.fastq.gz	Fastqsanger.gz
	SRR7868824_1.fastq.gz	Fastqsanger.gz
	SRR7868824_2.fastq.gz	Fastqsanger.gz
	SRR7868825_1.fastq.gz	Fastqsanger.gz

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Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription

Project description:Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription

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Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription [GRO-Seq]

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Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription [HiC-Seq]

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Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-Based Regulation of Transcription.

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Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription [GRO-Seq]

Project description:Increasing evidence suggests that transcriptional control and chromatin activities at large involve regulatory RNAs, which likely enlist specific RNA binding proteins (RBPs). Although multiple RBPs have been implicated in transcriptional control, it has remained unclear how extensively RBPs directly act on chromatin. We embarked on a large-scale RBP ChIP-seq analysis, revealing widespread RBP presence in active chromatin regions in the human genome. Like transcription factors (TFs), RBPs also showed strong preference for hotspots in the genome, particularly gene promoters, where their association is frequently linked to transcriptional output. Unsupervised clustering reveals extensive co-association between TFs and RBPs, as exemplified by YY1, a known RNA-dependent TF, and RBM25, an RBP involved in splicing regulation. Remarkably, RBM25 depletion attenuates all YY1-dependent activities, including chromatin binding, DNA looping and transcription. We propose that various RBPs may enhance network interaction through harnessing regulatory RNAs to control transcription. As part of the ENCODE consortium, we embarked on a large-scale RBP ChIP-seq analysis, revealing broad presence of RBPs in active chromatin regions in the human genome. Like transcription factors (TFs), RBPs also show great preference for hotspots in the genome, particularly gene promoters, where their binding is frequently linked to transcriptional output. Self-organizing map reveals extensive co-binding events between TFs and RBPs, as exemplified by those between YY1, a known RNA-dependent TF, and RBM25, an RBP involved in alternative splicing. Remarkably, RBM25 depletion attenuates all YY1-dependent activities, including chromatin binding, DNA looping and transcription. We propose that various RBPs may bridge specific TF-RNA interactions to control transcription.

2019-06-27 | GSE120105 | GEO

Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription [ChIP-Seq]

2019-06-27 | GSE120104 | GEO

Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-06-27 | GSE120110 | GEO

Selective enhancement and repression of glucocorticoid receptor signaling by coregulator Hic-5

Project description:The glucocorticoid receptor (GR) recruits many coregulators via the well characterized AF2 interaction surface in the GR ligand binding domain, but LIM domain coregulator Hic-5 binds to the relatively uncharacterized tau2 activation domain in the hinge region of GR. Requirement of Hic-5 for glucocorticoid-regulated gene expression in U2OS osteosarcoma cells was defined by Hic-5 depletion and global gene expression analysis. Hic-5 depletion had selective and dramatic effects, positive and negative, on both activation and repression of GR target genes. For some hormone-induced genes, Hic-5 facilitated recruitment of the Mediator complex and RNA polymerase II. In contrast, many genes were not regulated by hormone until Hic-5 was depleted. On these genes Hic-5 acted at a very early step of the regulatory process, preventing efficient GR binding on enhancers, chromatin remodeling, and thus preventing glucocorticoid-driven transcriptional regulation. Overall, Hic-5 has selective and diverse roles on GR target genes, functioning as coactivator on some genes and corepressor on others, and either facilitating or opposing the glucocorticoid-driven actions of GR. Hic-5 exhibits multiple mechanisms of action, either regulating GR binding to DNA and chromatin remodeling, or facilitating later steps in transcription complex assembly. We investigate the relationship between GR and Hic5 and identify classes of genes that respond differently when cells are induced with hormone and when Hic5 is knocked down We knock down Hic-5 (TGFB1I1) in U2OS cells using siRNA (siHic5_2) along with nonspecific siRNA (shNS) and assay gene expression changes at 4 different time points of hormone treatment. We also include non-infected control (NI) as a second control at each time point.

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