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Splicing of Ezh1 gets muscle out of stressful situations

Nature Structural & Molecular Biology volume 24, pages 435–437 (2017)Cite this article

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As cells undergo terminal differentiation, the composition of Polycomb-repressive complex 2 (PRC2) changes and the histone H3K27 methyltransferase Ezh2 is progressively replaced by its homolog Ezh1. By identifying an enzymatically inactive splice variant of Ezh1 that is sensitive to cellular stress, Bodega et al. now demonstrate that PRC2–Ezh1 has an essential role in establishing an altered gene expression program required for postmitotic muscle cells to adapt to environmental changes.

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Figure 1: Splicing of Ezh1 limits the level of functional PRC2 complex in healthy cells while allowing a rapid adaptive response to oxidative stress.

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Acknowledgements

Work in the Brand and Dilworth labs is supported by grants from the Canadian Institutes of Health Research (MOP-82813 to M.B. and FDN-143330 to F.J.D.).

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  1. and the Department of Cellular and Molecular Medicine, Marjorie Brand and F. Jeffrey Dilworth are at the Sprott Centre for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada, University of Ottawa, Ottawa, Ontario, Canada.,

    Marjorie Brand & F Jeffrey Dilworth

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  1. Marjorie Brand
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  2. F Jeffrey Dilworth
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Correspondence to Marjorie Brand or F Jeffrey Dilworth.

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Brand, M., Dilworth, F. Splicing of Ezh1 gets muscle out of stressful situations. Nat Struct Mol Biol 24, 435–437 (2017). https://doi.org/10.1038/nsmb.3406

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