Article
- The EMBO Journal (2006) 25, 3110 - 3122
- doi:10.1038/sj.emboj.7601187
Published online: 8 June 2006
Subject Category:
Recruitment of PRC1 function at the initiation of X inactivation independent of PRC2 and silencing
Stefan Schoeftner1, Aditya K Sengupta1, Stefan Kubicek1, Karl Mechtler1, Laura Spahn2, Haruhiko Koseki3, Thomas Jenuwein1 and Anton Wutz1
- Research Institute of Molecular Pathology, Vienna, Austria
- Centre of Molecular Medicine, Vienna, Austria
- RIKEN Research Center for Allergy and Immunology (RCAI), RIKEN Yokohama Institute, Suehiro, Tsurumi-ku, Yokohama, Japan
Correspondence to:
Anton Wutz, Research Institute of Molecular Pathology, Vienna Biocenter, Dr. Bohr-Gasse 7, 1030 Vienna, Austria. Tel.: +43 1 797 30 521; Fax: +43 1 798 87153; E-mail: wutz@imp.univie.ac.at
Received 4 October 2005; Accepted 17 May 2006
Abstract
In mammals X inactivation is initiated by expression of Xist RNA and involves the recruitment of Polycomb repressive complex 1 (PRC1) and 2 (PRC2), which mediate chromosome-wide ubiquitination of histone H2A and methylation of histone H3, respectively. Here, we show that PRC1 recruitment by Xist RNA is independent of gene silencing. We find that Eed is required for the recruitment of the canonical PRC1 proteins Mph1 and Mph2 by Xist. However, functional Ring1b is recruited by Xist and mediates ubiquitination of histone H2A in Eed deficient embryonic stem (ES) cells, which lack histone H3 lysine 27 tri-methylation. Xist expression early in ES cell differentiation establishes a chromosomal memory, which allows efficient H2A ubiquitination in differentiated cells and is independent of silencing and PRC2. Our data show that Xist recruits PRC1 components by both PRC2 dependent and independent modes and in the absence of PRC2 function is sufficient for the establishment of Polycomb-based memory systems in X inactivation.
Keywords:
- Eed,
- Polycomb,
- Ring1b,
- X inactivation,
- Xist
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