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Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domains

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

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE184466 | GEO | 2022/07/12

REPOSITORIES: GEO

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Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domains [Clr3-CDx2]

Project description:Clr3-CDx2 occupancy along fission yeast chromosomes. Chromodomain-mediated loading targets Clr3-CDx2 to heterochromatin domains.

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Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domains [H3K9me3 ChIP]

Project description:ChIP-chip analyses of lysine-9 trimethylated histone H3 in clr3-CDx2 and wild type cells. Chromodomain-mediated HDAC loading sustains self-templated propagation of extended heterochromatin domain.

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Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domains [H3-T7 ChIP]

Project description:ChIP-chip analyses of pulse-expressed H3-T7 in clr3-CDx2 and wild type cells Chromodomain-mediated HDAC loading suppresses histone turnover at self-templated heterochromatin domain. Chromodomain-mediated loading targets Clr3-CDx2 to heterochromatin domains.

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Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domain [ChIP-seq]

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Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domains

Project description:Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domains

| PRJNA764716 | ENA

Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domains [H3K9me3 ChIP]

Project description:Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domains [H3K9me3 ChIP]

| PRJNA764719 | ENA

Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domains [Clr3-CDx2]

Project description:Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domains [Clr3-CDx2]

| PRJNA833077 | ENA

Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domains [H3-T7 ChIP]

Project description:Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domains [H3-T7 ChIP]

| PRJNA764720 | ENA

Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domain [ChIP-seq]

Project description:Histone deacetylation primes chromatin to preserve epigenetic memory for self-propagation of heterochromatin domain [ChIP-seq]

| PRJNA833076 | ENA

Epigenetic gene silencing by heterochromatin primes fungal resistance.

Project description:Heterochromatin that depends on histone H3 lysine 9 methylation (H3K9me) renders embedded genes transcriptionally silent1-3. In the fission yeast Schizosaccharomyces pombe, H3K9me heterochromatin can be transmitted through cell division provided the counteracting demethylase Epe1 is absent4,5. Heterochromatin heritability might allow wild-type cells under certain conditions to acquire epimutations, which could influence phenotype through unstable gene silencing rather than DNA change6,7. Here we show that heterochromatin-dependent epimutants resistant to caffeine arise in fission yeast grown with threshold levels of caffeine. Isolates with unstable resistance have distinct heterochromatin islands with reduced expression of embedded genes, including some whose mutation confers caffeine resistance. Forced heterochromatin formation at implicated loci confirms that resistance results from heterochromatin-mediated silencing. Our analyses reveal that epigenetic processes promote phenotypic plasticity, letting wild-type cells adapt to unfavourable environments without genetic alteration. In some isolates, subsequent or coincident gene-amplification events augment resistance. Caffeine affects two anti-silencing factors: Epe1 is downregulated, reducing its chromatin association, and a shortened isoform of Mst2 histone acetyltransferase is expressed. Thus, heterochromatin-dependent epimutation provides a bet-hedging strategy allowing cells to adapt transiently to insults while remaining genetically wild type. Isolates with unstable caffeine resistance show cross-resistance to antifungal agents, suggesting that related heterochromatin-dependent processes may contribute to resistance of plant and human fungal pathogens to such agents.

| S-EPMC7116710 | biostudies-literature

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