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Background  X-chromosome inactivation occurs early in mammalian development and results in the inactive X chromosome acquiring numerous hallmarks of heterochromatin. While XIST is a key player in the inactivation process, the method of action of this ncRNA is yet to be determined.    Methodology/Principal Findings  To assess which features of heterochromatin may be directly recruited by the expression and localization of the XIST RNA we have analyzed a mouse/human somatic cell hybrid in which expression of human and mouse  XIST/Xist  has been induced from the active X by demethylation. Such hybrids had previously been demonstrated to disconnect  XIST/Xist  expression from gene silencing and we confirm maintenance of X-linked gene expression, even close to the  Xist  locus, despite the localized expression of mouse Xist.    Conclusions/Significance  Loss of the active chromatin marks H3 acetylation and H3 lysine 4 methylation was not observed upon  XIST/Xist  expression, nor was there a gain of DNA methylation; thus these marks of facultative heterochromatin are not solely dependent upon  Xist  expression. Cot-1 holes, regions of depleted RNA hybridization with a Cot-1 probe, were observed upon  Xist  expression; however, these were at reduced frequency and intensity in these somatic cells. Domains of human Cot-1 transcription were observed corresponding to the human chromosomes in the somatic cell hybrids. The Cot-1 domain of the X was not reduced with the expression of XIST, which fails to localize to the human X chromosome in a mouse somatic cell background. The human inactive X in a mouse/human hybrid cell also shows delocalized XIST expression and an ongoing Cot-1 domain, despite X-linked gene silencing. These results are consistent with recent reports separating Cot-1 silencing from genic silencing, but also demonstrate repetitive element expression from an otherwise silent X chromosome in these hybrid cells.

Active Chromatin Marks Are Retained on X Chromosomes Lacking Gene or Repeat Silencing Despite XIST/Xist Expression in Somatic Cell Hybrids