Xist RNA and the mechanism of X chromosome inactivation

Kathrin Plath, Susanna Mlynarczyk-Evans, Dmitri A. Nusinow, Barbara Panning

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381 Scopus citations


Dosage compensation in mammals is achieved by the transcriptional inactivation of one X chromosome in female cells. From the time X chromosome inactivation was initially described, it was clear that several mechanisms must be precisely integrated to achieve correct regulation of this complex process. X-inactivation appears to be triggered upon differentiation, suggesting its regulation by developmental cues. Whereas any number of X chromosomes greater than one is silenced, only one X chromosome remains active. Silencing on the inactive X chromosome coincides with the acquisition of a multitude of chromatin modifications, resulting in the formation of extraordinarily stable facultative heterochromatin that is faithfully propagated through subsequent cell divisions. The integration of all these processes requires a region of the X chromosome known as the X-inactivation center, which contains the Xist gene and its cis-regulatory elements. Xist encodes an RNA molecule that plays critical roles in the choice of which X chromosome remains active, and in the initial spread and establishment of silencing on the inactive X chromosome. We are now on the threshold of discovering the factors that regulate and interact with Xist to control X-inactivation, and closer to an understanding of the molecular mechanisms that underlie this complex process.

Original languageEnglish
Pages (from-to)233-278
Number of pages46
JournalAnnual Review of Genetics
StatePublished - 2002


  • Differentiation
  • Dosage compensation
  • Facultative heterochromatin
  • Imprinting
  • Tsix RNA


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