Cureus | HDAC mediated suppression of histone turnover promotes epigenetic stability of heterochromatin
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Research Article

HDAC mediated suppression of histone turnover promotes epigenetic stability of heterochromatin

Ozan Aygün, Sameet Mehta, Shiv I. S. Grewal

Published: May 01, 2013

DOI: 10.1038/nsmb.2565

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Abstract

Heterochromatin causes epigenetic repression that can be transmitted through multiple cell divisions. However, the mechanisms underlying silencing and stability of heterochromatin are not fully understood. We show that heterochromatin differs from euchromatin in histone turnover, and identify histone deacetylase (HDAC) Clr3 as a factor required for inhibiting histone turnover across heterochromatin domains in Schizosaccharomyces pombe. Loss of RNAi factors, Clr4 methyltransferase, or HP1 proteins involved in HDAC localization causes increased histone turnover across pericentromeric domains. Clr3 also affects histone turnover at the silent mating–type region where it can be recruited by alternative mechanisms acting in parallel to H3K9me–HP1. Importantly, the JmjC–domain protein Epe1 promotes histone exchange, and loss of Epe1 suppresses both histone turnover and defects in heterochromatic silencing. Our results suggest that heterochromatic silencing factors preclude histone turnover to promote silencing and inheritance of repressive chromatin.


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Scholarly Impact Quotient™ (SIQ™) is our unique post-publication peer review rating process. SIQ™ assesses article importance and quality by embracing the collective intelligence of the Cureus community-at-large. All registered users are invited to contribute to the SIQ™ of any published article. (Authors cannot rate their own articles.)

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