Role of Histone H3 Lysine 27 Methylation in X Inactivation

Author:

Plath Kathrin1,Fang Jia2,Mlynarczyk-Evans Susanna K.1,Cao Ru2,Worringer Kathleen A.1,Wang Hengbin2,de la Cruz Cecile C.1,Otte Arie P.3,Panning Barbara1,Zhang Yi2

Affiliation:

1. Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, CA 94143, USA.

2. Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599–7295, USA.

3. Swammerdam Institute for Life Sciences, BioCentrum Amsterdam, University of Amsterdam, 1018 TV Amsterdam, Netherlands.

Abstract

The Polycomb group (PcG) protein Eed is implicated in regulation of imprinted X-chromosome inactivation in extraembryonic cells but not of random X inactivation in embryonic cells. The Drosophila homolog of the Eed-Ezh2 PcG protein complex achieves gene silencing through methylation of histone H3 on lysine 27 (H3-K27), which suggests a role for H3-K27 methylation in imprinted X inactivation. Here we demonstrate that transient recruitment of the Eed-Ezh2 complex to the inactive X chromosome (Xi) occurs during initiation of X inactivation in both extraembryonic and embryonic cells and is accompanied by H3-K27 methylation. Recruitment of the complex and methylation on the Xi depend on Xist RNA but are independent of its silencing function. Together, our results suggest a role for Eed-Ezh2–mediated H3-K27 methylation during initiation of both imprinted and random X inactivation and demonstrate that H3-K27 methylation is not sufficient for silencing of the Xi.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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