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Nat Struct Mol Biol. 2017 May;24(5):444-452. doi: 10.1038/nsmb.3392. Epub 2017 Mar 27.

A cytosolic Ezh1 isoform modulates a PRC2-Ezh1 epigenetic adaptive response in postmitotic cells.

Author information

1
Istituto Nazionale di Genetica Molecolare (INGM) Romeo and Enrica Invernizzi, Milan, Italy.
2
IRCSS Fondazione Santa Lucia, Epigenetics and Genome Reprogramming, Rome, Italy.
3
Environmental Epigenetics Research Program, Division of Biological Environmental Sciences and Engineering, King Abdullah University of Science and Technology (KAUST), Thuwal, Saudi Arabia.
4
Dulbecco Telethon Institute at San Raffaele Scientific Institute, Milan, Italy.
5
Génétique et Biologie du Développement, Institut Curie, Inserm, Paris, France.
6
CNR Institute of Cellular Biology and Neurobiology, Rome, Italy.

Abstract

The evolution of chromatin-based epigenetic cell memory may be driven not only by the necessity for cells to stably maintain transcription programs, but also by the need to recognize signals and allow plastic responses to environmental stimuli. The mechanistic role of the epigenome in adult postmitotic tissues, however, remains largely unknown. In vertebrates, two variants of the Polycomb repressive complex (PRC2-Ezh2 and PRC2-Ezh1) control gene silencing via methylation of histone H3 on Lys27 (H3K27me). Here we describe a reversible mechanism that involves a novel isoform of Ezh1 (Ezh1β). Ezh1β lacks the catalytic SET domain and acts in the cytoplasm of skeletal muscle cells to control nuclear PRC2-Ezh1 activity in response to atrophic oxidative stress, by regulating Eed assembly with Suz12 and Ezh1α (the canonical isoform) at their target genes. We report a novel PRC2-Ezh1 function that utilizes Ezh1β as an adaptive stress sensor in the cytoplasm, thus allowing postmitotic cells to maintain tissue integrity in response to environmental changes.

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PMID:
28346433
DOI:
10.1038/nsmb.3392
[Indexed for MEDLINE]

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