Role of Histone H3 Lysine 27 Methylation in X Inactivation

Kathrin Plath(University of California, San Francisco), Jia Fang(University of North Carolina at Chapel Hill), Susanna Mlynarczyk‐Evans(University of California, San Francisco), Ru Cao(University of North Carolina at Chapel Hill), Kathleen A. Worringer(University of California, San Francisco), Hengbin Wang(University of North Carolina at Chapel Hill), Cecile C. de la Cruz(University of California, San Francisco), Arie P. Otte(Amsterdam University of Applied Sciences), Barbara Panning(University of California, San Francisco), Yi Zhang(University of North Carolina at Chapel Hill)
Science
April 4, 2003
10.1126/science.1084274
Cited by 1,188

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.

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