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Science 19 September 2008:
Vol. 321. no. 5896, pp. 1693 - 1695
DOI: 10.1126/science.1160952
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Reports

Molecular Coupling of Xist Regulation and Pluripotency

Pablo Navarro,1 Ian Chambers,2 Violetta Karwacki-Neisius,2 Corinne Chureau,1 Céline Morey,1 Claire Rougeulle,1* Philip Avner1*

During mouse embryogenesis, reversion of imprinted X chromosome inactivation in the pluripotent inner cell mass of the female blastocyst is initiated by the repression of Xist from the paternal X chromosome. Here we report that key factors supporting pluripotency—Nanog, Oct3/4, and Sox2—bind within Xist intron 1 in undifferentiated embryonic stem (ES) cells. Whereas Nanog null ES cells display a reversible and moderate up-regulation of Xist in the absence of any apparent modification of Oct3/4 and Sox2 binding, the drastic release of all three factors from Xist intron 1 triggers rapid ectopic accumulation of Xist RNA. We conclude that the three main genetic factors underlying pluripotency cooperate to repress Xist and thus couple X inactivation reprogramming to the control of pluripotency during embryogenesis.

1 Institut Pasteur, Unité de Génétique Moléculaire Murine, CNRS, URA2578, F-75015, Paris, France.
2 Medical Research Council (MRC) Centre Development in Stem Cell Biology, Institute for Stem Cell Research, School of Biological Sciences, University of Edinburgh, MRC EH9 3JQ, Edinburgh, UK.

* To whom correspondence should be addressed. E-mail: rougeull{at}pasteur.fr (C.R.); pavner{at}pasteur.fr (P.A.)

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Lessons from X-chromosome inactivation: long ncRNA as guides and tethers to the epigenome.
J. T. Lee (2009)
Genes & Dev. 23, 1831-1842
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The transcriptional foundation of pluripotency.
I. Chambers and S. R. Tomlinson (2009)
Development 136, 2311-2322
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Science. ISSN 0036-8075 (print), 1095-9203 (online)