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Histone H3.3 ensures cell proliferation and genomic stability during myeloid cell development [CUT&RUN]

ABSTRACT: Histone H3.3 ensures cell proliferation and genomic stability during myeloid cell development [CUT&RUN]

PROVIDER: PRJNA1201232 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31797751_1.fastq.gz	Fastqsanger.gz
	SRR31797751_2.fastq.gz	Fastqsanger.gz
	SRR31797752_1.fastq.gz	Fastqsanger.gz
	SRR31797752_2.fastq.gz	Fastqsanger.gz
	SRR31797753_1.fastq.gz	Fastqsanger.gz

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Histone H3.3 ensures cell proliferation and genomic stability during myeloid cell development [RNA-seq]

Project description:Histone H3.3 ensures cell proliferation and genomic stability during myeloid cell development [RNA-seq]

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Histone H3.3 ensures cell proliferation and genomic stability during myeloid cell development [ATAC-seq]

Project description:Histone H3.3 ensures cell proliferation and genomic stability during myeloid cell development [ATAC-seq]

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Histone H3.3 ensures cell proliferation and genomic stability during myeloid cell development [CUT&RUN]

Project description:Variant histone H3.3 is thought to be critical for survival of many cells, since it is deposited in expressed genes, a feature different from core histones. For example, H3.3 deletion leads to embryonic lethality in mice. However, requirement of H3.3 in later stage of development has remained unclear. The aim of this work was to elucidate the role of H3.3 for development of myeloid lineage, important for innate immunity. We conditionally knocked out (cKO) the H3.3 genes in myeloid progenitor cells differentiating into bone marrow derived macrophages (BMDMs). Progenitor cells lacking H3.3 were defective in replication, suffered from extensive DNA damage, and underwent apoptosis. Surviving H3.3cKO cells expressed many interferon stimulated genes (ISGs) throughout differentiation. Further, H3.3cKO BMDMs possessed chromatin accessible sites, and histone posttranslational modifications consistent with the gene expression profiles, Accordingly, H3.3cKO BMDMs retained general nucleosomal structure genome wide. In summary, H3.3 is required for proliferation of myeloid progenitor cells, but is in large part dispensable for differentiation of BMDMs.

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Histone H3.3 ensures cell proliferation and genomic stability during myeloid cell development [ATAC-seq]

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Histone H3.3 is required for endogenous retroviral element silencing and genome stability [RNA-Seq]

Project description:Endogenous retroviruses (ERVs) have provided an evolutionary advantage in the diversification of transcript regulation and are thought to be involved in the establishment of extraembryonic tissues during development. However, silencing of these elements remains critical for the maintenance of genome stability. Here, we define a new chromatin state that is uniquely characterized by the combination of the histone variant H3.3 and H3K9me3, two chromatin ‘marks’ that have previously been considered to belong to fundamentally opposing chromatin states. H3.3/H3K9me3 heterochromatin is fundamentally distinct from ‘canonical’ H3K9me3 heterochromatin that has been under study for decades and this unique functional interplay of a histone variant and a repressive histone mark is crucial for silencing ERVs in ESCs. Our study solidifies the emerging notion that H3.3 is not a histone variant associated exclusively with “active” chromatin and further suggests that its incorporation at unique heterochromatic regions may be central to its function during development and the maintenance of genome stability. RNA-seq analysis of three embryonic stem cell lines WT, H3.3 KO1, and H3.3 KO2)

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Profiling of H3.3

Project description:Histone variants can effect nucleosome stability or affect histone of DNA modifications. H3.3 is a major H3 histone variant that is incorporated into chromatin outside of S-phase in various eukaryotes. In animals, H3.3 is associated with active transcription and possibly maintenance of transcriptional memory. Plant H3.3, which evolved independently of animal H3.3, is much less well understood. We performed ChIP-chip using chromatin from rosette leaves of 35S:H3.3-YFP plants.

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R-loop dependent promoter-proximal termination ensures genome stability

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Epigenetic regulation of DNA repair pathway choice by macroH2A1 splice variants ensures genome stability

Project description:Epigenetic regulation of DNA repair pathway choice by macroH2A1 splice variants ensures genome stability

2020-06-03 | MSV000085541 | MassIVE

Factors influencing in vivo deposition of histone variants H3.1 and H3.3

Project description:Establishment of a proper chromatin landscape is central to genome function. Here, we explain H3 variant distribution by specific targeting and dynamics of deposition involving the CAF-1 and HIRA histone chaperones. Impairing replicative H3.1 incorporation via CAF-1 enables an alternative H3.3 deposition at replication sites via HIRA. Conversely, the H3.3 incorporation throughout the cell cycle via HIRA cannot be replaced by H3.1. ChIP-seq analyses reveal correlation between HIRA-dependent H3.3 accumulation and RNA pol II at transcription sites and specific regulatory elements, further supported by their biochemical association. Remarkably, the HIRA complex shows unique DNA binding properties and depleting HIRA increases DNA sensitivity to nucleases. We propose that protective gap-filling of naked DNA by HIRA leads to a broad distribution of H3.3, and HIRA association with Pol II ensures local H3.3 enrichment at specific sites. Examination of genome-wide localization of two histone H3 variants.

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