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Recruitment of PRC1 function at the initiation of X inactivation independent of PRC2 and silencing
Author(s) -
Schoeftner Stefan,
Sengupta Aditya K,
Kubicek Stefan,
Mechtler Karl,
Spahn Laura,
Koseki Haruhiko,
Jenuwein Thomas,
Wutz Anton
Publication year - 2006
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7601187
Subject(s) - xist , prc2 , biology , x inactivation , histone , histone h2a , histone h3 , gene silencing , microbiology and biotechnology , histone methylation , polycomb group proteins , genetics , dna methylation , gene expression , x chromosome , gene , repressor
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.