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Different Chromatin and DNA Sequence Characteristics Define Glucocorticoid Receptor Binding Sites that are Blocked or Not Blocked by Coregulator Hic-5 [ChIP-seq]

ABSTRACT: Different Chromatin and DNA Sequence Characteristics Define Glucocorticoid Receptor Binding Sites that are Blocked or Not Blocked by Coregulator Hic-5 [ChIP-seq]

PROVIDER: PRJNA430719 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6497520.fastq.gz	Fastqsanger.gz
	SRR6497530.fastq.gz	Fastqsanger.gz
	SRR6497521.fastq.gz	Fastqsanger.gz
	SRR6497531.fastq.gz	Fastqsanger.gz
	SRR6497522.fastq.gz	Fastqsanger.gz

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Different Chromatin and DNA Sequence Characteristics Define Glucocorticoid Receptor Binding Sites that are Blocked or Not Blocked by Coregulator Hic-5 [ATAC-seq]

Project description:The glucocorticoid-activated glucocorticoid receptor (GR) regulates cellular stress pathways by binding to genomic regulatory elements of target genes and recruiting coregulator proteins to remodel chromatin and regulate transcription complex assembly. The coregulator Hydrogen peroxide-inducible clone 5 (Hic-5) is required for glucocorticoid regulation of some genes, but not others, and blocks regulation of a third gene set. Hic-5 inhibits GR binding to blocked genes but not other glucocorticoid-regulated genes. Site-specific blocking of GR binding is due to gene-specific requirements for ATP-dependent chromatin remodeling enzymes. We investigate the effects of Hic-5 and dexamethasone on chromatin accessibility at GR binding sites near Hic-5 blocked genes and non-blocked genes.

2018-05-08 | GSE109589 | GEO

Different Chromatin and DNA Sequence Characteristics Define Glucocorticoid Receptor Binding Sites that are Blocked or Not Blocked by Coregulator Hic-5 [ChIP-seq]

Project description:The glucocorticoid-activated glucocorticoid receptor (GR) regulates cellular stress pathways by binding to genomic regulatory elements of target genes and recruiting coregulator proteins to remodel chromatin and regulate transcription complex assembly. The coregulator Hydrogen peroxide-inducible clone 5 (Hic-5) is required for glucocorticoid regulation of some genes, but not others, and blocks regulation of a third gene set. Hic-5 inhibits GR binding to blocked genes but not other glucocorticoid-regulated genes. Site-specific blocking of GR binding is due to gene-specific requirements for ATP-dependent chromatin remodeling enzymes. We investigate whether ATPases CHD9 and BRM were required for GR occupancy at GR binding sites near Hic-5 blocked genes.

2018-05-08 | GSE109383 | GEO

Different Chromatin and DNA Sequence Characteristics Define Glucocorticoid Receptor Binding Sites that are Blocked or Not Blocked by Coregulator Hic-5

Project description:Different Chromatin and DNA Sequence Characteristics Define Glucocorticoid Receptor Binding Sites that are Blocked or Not Blocked by Coregulator Hic-5

| PRJNA431430 | ENA

Different Chromatin and DNA Sequence Characteristics Define Glucocorticoid Receptor Binding Sites that are Blocked or Not Blocked by Coregulator Hic-5 [ATAC-seq]

Project description:Different Chromatin and DNA Sequence Characteristics Define Glucocorticoid Receptor Binding Sites that are Blocked or Not Blocked by Coregulator Hic-5 [ATAC-seq]

| PRJNA431440 | ENA

Different chromatin and DNA sequence characteristics define glucocorticoid receptor binding sites that are blocked or not blocked by coregulator Hic-5.

Project description:The glucocorticoid receptor (GR) regulates genes in many physiological pathways by binding to enhancer and silencer elements of target genes, where it recruits coregulator proteins that remodel chromatin and regulate the assembly of transcription complexes. The coregulator Hydrogen peroxide-inducible clone 5 (Hic-5) is necessary for glucocorticoid (GC) regulation of one group of GR target genes, is irrelevant for a second group, and inhibits GR binding to a third gene set, thereby blocking their regulation by GC. Gene-specific characteristics that distinguish GR binding regions (GBR) at Hic-5 blocked genes from GBR at other GC-regulated genes are unknown. Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5. Furthermore blocked GBR are in a closed conformation prior to Hic-5 depletion, and require Hic-5 depletion and glucocorticoid treatment to create an open conformation necessary for GR occupancy. A transcription factor binding motif characteristic of the ETS family was enriched near blocked GBR and blocked genes but not near non-blocked GBR or non-blocked GR target genes. Thus, we identify specific differences in chromatin conformation, chromatin remodeler requirements, and local DNA sequence motifs that contribute to gene-specific actions of transcription factors and coregulators. These findings shed light on mechanisms that contribute to binding site selection by transcription factors, which vary in a cell type-specific manner.

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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.

2014-03-21 | E-GEOD-46448 | biostudies-arrayexpress

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

2014-03-21 | GSE46448 | GEO

Different Chromatin and DNA Sequence Characteristics Define Glucocorticoid Receptor Binding Sites that are Blocked or Not Blocked by Coregulator Hic-5

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

2018-05-08 | GSE109590 | GEO

Selective coregulator function for different steroid receptors and restriction of steroid receptor chromatin occupancy by Hic-5 (GRÎ³)

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 two different siRNA (siHic5_2 and siHic5_5) 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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Selective coregulator function for different steroid receptors and restriction of steroid receptor chromatin occupancy by Hic-5 (GRγ)

2016-01-01 | GSE65401 | GEO