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Hormone induced repression of genes requires BRG1-mediated H1.2 deposition at target promoters

ABSTRACT: In this report we have discovered a new function of BRG1 during hormone-mediated gene repression. The ATPase BRG1 without the other subunits of the BAF complex is recruited by the hormone receptor to genomic sites marked by the pioneering factor FOXA1, where it remodels the target chromatin by interacting with linker histone H1.2 facilitating its deposition.

ORGANISM(S): Homo sapiens

PROVIDER: GSE83785 | GEO | 2016/07/11

SECONDARY ACCESSION(S): PRJNA326976

REPOSITORIES: GEO

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Hormone-induced repression of genes requires BRG1-mediated H1.2 deposition at target promoters.

Project description:Eukaryotic gene regulation is associated with changes in chromatin compaction that modulate access to DNA regulatory sequences relevant for transcriptional activation or repression. Although much is known about the mechanism of chromatin remodeling in hormonal gene activation, how repression is accomplished is much less understood. Here we report that in breast cancer cells, ligand-activated progesterone receptor (PR) is directly recruited to transcriptionally repressed genes involved in cell proliferation along with the kinases ERK1/2 and MSK1. PR recruits BRG1 associated with the HP1γ-LSD1 complex repressor complex, which is further anchored via binding of HP1γ to the H3K9me3 signal deposited by SUV39H2. In contrast to what is observed during gene activation, only BRG1 and not the BAF complex is recruited to repressed promoters, likely due to local enrichment of the pioneer factor FOXA1. BRG1 participates in gene repression by interacting with H1.2, facilitating its deposition and stabilizing nucleosome positioning around the transcription start site. Our results uncover a mechanism of hormone-dependent transcriptional repression and a novel role for BRG1 in progestin regulation of breast cancer cell growth.

| S-EPMC5010049 | biostudies-literature

ChIP-seq for histone H1.2 in A549

Project description:Our study represents the detailed analysis of whole-genome DNA-binding sites of linker histone variant H1.2 in human lung cancer cell line A549, with biologic replicates, generated by ChIP-seq technology

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Linker histone H1.2 establishes chromatin comapction and gene silencing through recognition of H3K27me3

Project description:Linker histone H1 is a protein component of chromatin and has been linked to chromatin compaction and global gene silencing.It has been sugegsted that H1 plays a significant role, regulating a relatively small number of genes. Here we show that H1.2- a variant of H1 subtype is recruited to chromatin region and is dependent on EZH2-mediated H3K27me3. Therefore a Gene expression array analysis was carried out with H1.2 as well as EZH2 knockout MCF7 cells to confirm the interlationship of H1.2 and EZH2 activity. Total RNA was isolated from MCF7 cells in which EZH2 and H1.2 genes have been depleted along with the wild type cells to study the differential regulation of various genes in each case.

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Protein-protein interactions of BRG1 or BRG1-HSA in SW13 cells

Project description:The SWI/SNF complex remodels chromatin in an ATP-dependent manner through the ATPase subunits BRG1 and BRM. Chromatin remodeling alters nucleosome structure to change gene expression, however aberrant remodeling and gene expression can result in cancer. The function and localization on chromatin of the SWI/SNF complex depends on the protein makeup of the complex. Here we report the protein-protein interactions of wild-type BRG1 or mutant BRG1 in which the HSA domain has been deleted (BRG1-HSA). We demonstrate the interaction of BRG1 with most SWI/SNF complex members and a failure of a number of these members to interact with BRG1-HSA. These results demonstrate that the HSA domain of BRG1 is a critical interaction platform for the correct formation of SWI/SNF remodeling complexes.

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Genome-wide expression profiling in 293T cells upon depletion of H1.2, Cul4A or PAF1

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Linker histone H1.2 establishes chromatin comapction and gene silencing through recognition of H3K27me3

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The linker histone H1.2 directs the genome-wide chromatin-association and facilitates the biological effects of the retinoblastoma tumour suppressor protein

Project description:ChIPseq of Retinoblastoma protein in MCF7 cells in which linker histone H1.2 has been knocked down.

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Genome-wide expression profiling in 293T cells upon depletion of H1.2, Cul4A or PAF1

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ChIP-seq for histone H1.2 in iWAT of C57BL/6 mice under normal conditions or upon cold exposure

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The pioneer factor OCT4 requires the chromatin remodeller BRG1 to support gene regulatory element function in mouse embryonic stem cells [RNA-Seq]

Project description:Pioneer transcription factors are able to recognise and bind their motif sequences in inaccessible or closed chromatin, and their ability to achieve this is required to establish new regulatory elements and transcriptional networks during development and cellular reprogramming. An essential feature of this pioneering activity is the transition from inaccessible chromatin to a nucleosome-depleted and accessible chromatin state typical of normal regulatory elements, and this is believed to facilitate further transcription factor binding events. However, the mechanisms by which many pioneer transcription factors achieve this remarkable feat remain elusive. Here we reveal that the pluripotency-associated pioneer factor OCT4 binds inaccessible chromatin to shape the chromatin accessibility, transcription factor co-binding and regulatory potential of thousands of distal regulatory elements in mouse embryonic stem cells, demonstrating that its pioneering activity is a feature of normal pluripotency, and not just reprogramming. The accessible chromatin formed at OCT4 binding sites relies on the chromatin remodelling factor BRG1, which is recruited to these sites by OCT4. The occupancy of BRG1 is then required to support OCT4/SOX2 co-binding and normal expression of the pluripotency-associated transcriptome, and this reliance on BRG1 reflects OCT4 binding dynamics during cellular reprograming and early mouse development. Together these observations reveal a distinct requirement for the chromatin remodelling factor BRG1 in shaping the pioneering activity of OCT4 and regulating the pluripotency network in embryonic stem cells.

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