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The embryonic linker histone dBigH1 compromises the functional epigenetic state of active chromatin

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE127227 | GEO | 2020/02/20

REPOSITORIES: GEO

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The embryonic linker histone dBigH1 alters the functional state of active chromatin.

Project description:Linker histones H1 are principal chromatin components, whose contribution to the epigenetic regulation of chromatin structure and function is not fully understood. In metazoa, specific linker histones are expressed in the germline, with female-specific H1s being normally retained in the early-embryo. Embryonic H1s are present while the zygotic genome is transcriptionally silent and they are replaced by somatic variants upon activation, suggesting a contribution to transcriptional silencing. Here we directly address this question by ectopically expressing dBigH1 in Drosophila S2 cells, which lack dBigH1. We show that dBigH1 binds across chromatin, replaces somatic dH1 and reduces nucleosome repeat length (NRL). Concomitantly, dBigH1 expression down-regulates gene expression by impairing RNApol II binding and histone acetylation. These effects depend on the acidic N-terminal ED-domain of dBigH1 since a truncated form lacking this domain binds across chromatin and replaces dH1 like full-length dBigH1, but it does not affect NRL either transcription. In vitro reconstitution experiments using Drosophila preblastodermic embryo extracts corroborate these results. Altogether these results suggest that the negatively charged N-terminal tail of dBigH1 alters the functional state of active chromatin compromising transcription.

| S-EPMC7192587 | biostudies-literature

The embryonic linker histone dBigH1 compromises the functional epigenetic state of active chromatin [Affy]

Project description:Expression data from S2 cells wild type and expressing dBigH1

2020-02-17 | GSE127226 | GEO

The embryonic linker histone dBigH1 compromises the functional epigenetic state of active chromatin [ChIP2]

Project description:Genome wide distribution of dBigH1 and dH1 in cells expressing dBigH1ΔED. Genome wide distribution of Rpb3 in wild type S2 cells, cells expressing dBigH1 and cells expressing dBigH1ΔED.

2020-02-17 | GSE127225 | GEO

The embryonic linker histone dBigH1 compromises the functional epigenetic state of active chromatin [ChIP1]

Project description:Genome wide distribution of dBigH1 and dH1 in wild type cells and cells expressing dBigH1

2020-02-17 | GSE127224 | GEO

The embryonic linker histone dBigH1 compromises the functional epigenetic state of active chromatin

Project description:The embryonic linker histone dBigH1 compromises the functional epigenetic state of active chromatin

| PRJNA524369 | ENA

The embryonic linker histone dBigH1 compromises the functional epigenetic state of active chromatin [ChIP1]

Project description:The embryonic linker histone dBigH1 compromises the functional epigenetic state of active chromatin [ChIP1]

| PRJNA524366 | ENA

The embryonic linker histone dBigH1 compromises the functional epigenetic state of active chromatin [ChIP2]

Project description:The embryonic linker histone dBigH1 compromises the functional epigenetic state of active chromatin [ChIP2]

| PRJNA524367 | ENA

The embryonic linker histone dBigH1 compromises the functional epigenetic state of active chromatin [Affy]

Project description:The embryonic linker histone dBigH1 compromises the functional epigenetic state of active chromatin [Affy]

| PRJNA524368 | ENA

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

A Prion Epigenetic Switch Establishes an Active Chromatin State.

Project description:Covalent modifications to histones are essential for development, establishing distinct and functional chromatin domains from a common genetic sequence. Whereas repressed chromatin is robustly inherited, no mechanism that facilitates inheritance of an activated domain has been described. Here, we report that the Set3C histone deacetylase scaffold Snt1 can act as a prion that drives the emergence and transgenerational inheritance of an activated chromatin state. This prion, which we term [ESI+] for expressed sub-telomeric information, is triggered by transient Snt1 phosphorylation upon cell cycle arrest. Once engaged, the prion reshapes the activity of Snt1 and the Set3C complex, recruiting RNA pol II and interfering with Rap1 binding to activate genes in otherwise repressed sub-telomeric domains. This transcriptional state confers broad resistance to environmental stress, including antifungal drugs. Altogether, our results establish a robust means by which a prion can facilitate inheritance of an activated chromatin state to provide adaptive benefit.

| S-EPMC7195540 | biostudies-literature

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