An embryonic story: analysis of the gene regulative network controlling Xist expression in mouse embryonic stem cells.
In mice, dosage compensation of X-linked gene expression is achieved through the inactivation of one of the two X-chromosomes in XX female cells. The complex epigenetic process leading to X-inactivation is largely controlled by Xist and Tsix, two non-coding genes of opposing function. Xist RNA triggers X-inactivation by coating the inactive X, while Tsix is critical for the designation of the active X-chromosome through cis-repression of Xist RNA accumulation. Recently, a plethora of trans-acting factors and cis-regulating elements have been suggested to act as key regulators of either Xist, Tsix or both; these include ubiquitous factors such as Yy1 and Ctcf, developmental proteins such as Nanog, Oct4 and Sox2, and X-linked regulators such as Rnf12. In this paper we summarise recent advances in our knowledge of the regulation of Xist and Tsix in embryonic stem (ES) and differentiating ES cells.
Navarro
Pablo
P
Institut Pasteur, Unité de Génétique Moléculaire Murine, CNRS URA2578, Paris, France.
Avner
Philip
P
D000818:Animals; D002843:Chromatin / Q000378:metabolism; D004622:Embryo, Mammalian / Q000378:metabolism*; D053595:Embryonic Stem Cells / Q000378:metabolism*; D018507:Gene Expression Regulation, Developmental; D051379:Mice; D062085:RNA, Long Noncoding; D022661:RNA, Untranslated / Q000235:genetics* / Q000378:metabolism; D049951:X Chromosome Inactivation / Q000235:genetics
D002843:Chromatin; D062085:RNA, Long Noncoding; D022661:RNA, Untranslated; C077885:XIST non-coding RNA