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

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

PROVIDER: PRJNA420410 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6331570_1.fastq.gz	Fastqsanger.gz
	SRR6331570_2.fastq.gz	Fastqsanger.gz
	SRR6331580_1.fastq.gz	Fastqsanger.gz
	SRR6331580_2.fastq.gz	Fastqsanger.gz
	SRR6331590_1.fastq.gz	Fastqsanger.gz

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

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.

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

Project description:Genome Wide Distribution of Linker Histone H1.0 is Independent of MeCP2

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Genome-wide distribution of linker histone H1.0 is independent of MeCP2.

Project description:Previous studies suggested that MeCP2 competes with linker histone H1, but this hypothesis has never been tested in vivo. Here, we performed chromatin immunoprecipitation followed by sequencing (ChIP-seq) of Flag-tagged-H1.0 in mouse forebrain excitatory neurons. Unexpectedly, Flag-H1.0 and MeCP2 occupied similar genomic regions and the Flag-H1.0 binding was not changed upon MeCP2 depletion. Furthermore, mild overexpression of H1.0 did not alter MeCP2 binding, suggesting that the functional binding of MeCP2 and H1.0 are largely independent.

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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.

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

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

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