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Dynamic regulation of the histone variant H1.0 contributes to intratumor epigenetic and functional heterogeneity [RNA-Seq]

ABSTRACT: Identification of genes regulated by the histone variant H1.0 by RNA-seq analysis of cell lines expressing inducible specific shRNAs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE65518 | GEO | 2016/05/01

SECONDARY ACCESSION(S): PRJNA274266

REPOSITORIES: GEO

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Dynamic regulation of the histone variant H1.0 contributes to intratumor epigenetic and functional heterogeneity

Project description:Dynamic regulation of the histone variant H1.0 contributes to intratumor epigenetic and functional heterogeneity

| PRJNA274263 | ENA

The linker histone H1.0 generates epigenetic and functional intratumor heterogeneity

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2016-09-29 | GSE66169 | GEO

Dynamic regulation of the histone variant H1.0 contributes to intratumor epigenetic and functional heterogeneity

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

2016-05-01 | GSE65520 | GEO

The linker histone H1.0 generates epigenetic and functional intratumor heterogeneity [ChIP-Seq]

Project description:Identification of enrichment for H3K27ac and H3K27me3 in in vitro generated CSCs, following the knockdown of the histone linker H1.0

2016-09-30 | GSE73580 | GEO

The linker histone H1.0 generates epigenetic and functional intratumor heterogeneity [FAIRE-Seq]

Project description:Identification of nucleosome-free, active regulatory regions in in vitro generated CSCs, following the knockdown of the histone linker H1.0

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Dynamic regulation of the histone variant H1.0 contributes to intratumor epigenetic and functional heterogeneity [FAIRE-Seq]

Project description:Identification of nucleosome-free, active regulatory regions in in vitro generated CSCs and their parental hTERT-immortalized cell line.

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The linker histone H1.0 generates epigenetic and functional intratumor heterogeneity.

Project description:Tumors comprise functionally diverse subpopulations of cells with distinct proliferative potential. Here, we show that dynamic epigenetic states defined by the linker histone H1.0 determine which cells within a tumor can sustain the long-term cancer growth. Numerous cancer types exhibit high inter- and intratumor heterogeneity of H1.0, with H1.0 levels correlating with tumor differentiation status, patient survival, and, at the single-cell level, cancer stem cell markers. Silencing of H1.0 promotes maintenance of self-renewing cells by inducing derepression of megabase-sized gene domains harboring downstream effectors of oncogenic pathways. Self-renewing epigenetic states are not stable, and reexpression of H1.0 in subsets of tumor cells establishes transcriptional programs that restrict cancer cells' long-term proliferative potential and drive their differentiation. Our results uncover epigenetic determinants of tumor-maintaining cells.

| S-EPMC5131846 | biostudies-literature

Genome Wide Distribution of Linker Histone H1.0 is Independent of MeCP2 I

Project description:Previous studies suggested that MeCP2 binds to linker DNA and competes with linker histone H1 to regulate chromatin structure, but this hypothesis has never been tested in vivo. Here, we expressed Flag-tagged H1.0 in forebrain excitatory neurons in mice and performed ChIP-Seq to reveal H1.0 distribution and its relationship with MeCP2. Unexpectedly, we detected no major change in H1.0 upon MeCP2 depletion, revealing that MeCP2 functions independent of linker H1.0.

2018-05-28 | GSE95471 | GEO

Genome Wide Distribution of Linker Histone H1.0 is Independent of MeCP2 II

2018-05-28 | GSE107519 | GEO

Linker Histone H1.0 Couples Cellular Stiffness to Chromatin Structure [RNA-seq]

Project description:Eukaryotic nuclei encase the genome and differentially package it for the various needs of distinct cell types. Tuning of genome structure and function is accomplished by chromatin binding proteins, which are responsive to cellular stress, determining the transcriptome and phenotype of the cell. We sought to investigate the connection between extracellular stress and chromatin structure to regulate cellular stiffness. We demonstrate that the linker histone H1.0, which compacts nucleosomes into higher order chromatin fibers, controls genome structure and cellular response to stress. Histone H1.0 has privileged expression in tension-responsive fibroblasts across tissue types in mouse and humans, and is necessary and sufficient to mount a myofibroblast phenotype in these cells. Loss of histone H1.0 prevents transforming growth factor beta (TGF-b)-induced fibroblast contraction, proliferation and migration in an isoform-specific manner via inhibition of a transcriptome targeting extracellular matrix molecules. Histone H1.0 is associated with local regulation of gene expression by chromatin fiber compaction and histone acetylation, rendering the nucleus and cell stiffer in response to cytokine stimulation. Knockdown of H1.0 decreased levels of HDAC1 and the chromatin reader BRD4, thereby preventing transcription of a fibrotic gene program. Transient depletion of histone H1.0 in vivo decompacts chromatin and prevents fibrosis in cardiac muscle, lung, and kidney, thereby linking chromatin structure with fibroblast phenotype in response to extracellular stress. Our work identifies an unexpected role of linker histones to sense and respond to cellular stress, directly coupling cellular tension, nuclear organization and gene transcription.

2024-02-28 | GSE215267 | GEO

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