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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: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE109383 | GEO | 2018/05/08

REPOSITORIES: GEO

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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.

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Chromatin remodelers CHD9 and BRM are required for dex-regulated expression of block genes in U2OS-GR⍺ cells

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 glucocorticoid-regulated expression of Hic-5 blocked genes.

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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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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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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]

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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]

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

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ChIP-MS of GR and GR-DZn in mouse embryonic fibroblasts

Project description:The Glucocorticoid Receptor (GR) is both one of the most widely used clinical drug targets and a very potent metabolic regulator. GR belongs to the nuclear hormone receptor family of ligand-gated transcription factors that govern mammalian physiology. Upon ligand binding, GR enters the nucleus to regulate gene expression both positively and negatively. It is known to bind to consensus DNA sequences termed glucocorticoid response elements (GREs), but the mechanisms determining transcriptional activation versus repression remain an unresolved molecular paradox. Prevailing models suggest that tethering of GR to AP-1 or NF-κB via protein-protein interactions, rather than direct DNA binding, specifies negative regulation. However, here we show that the repression of inflammatory genes as well as all other glucocorticoid responses, require direct DNA binding of GR. Generating GR point mutant mice that retain the ability to tether via protein-protein interactions while unable to recognize DNA sequences, we demonstrate that response element recognition via the Zinc finger is absolutely required for both transcriptional activation and repression. We have used ChIP-Seq and RNA-Seq in inflammatory and metabolic cells and tissues together with proteomics to reveal that DNA binding of GR is necessary for the assembly of a functional SWI/SNF coregulator complex. Generally, the desired anti-inflammatory actions of GR are attributed to the silencing of inflammatory genes, while its adverse effects are believed to result from the transcriptional upregulation of metabolic targets. Our findings not only challenge classical models and dogmas of GR mediated gene regulation, but will provide an important basis for the development of novel immunosuppressants with reduced side effect profiles.

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