Jarid2 Is Implicated in the Initial Xist-Induced Targeting of PRC2 to the Inactive X Chromosome

Mol Cell. 2014 Jan 23;53(2):301-16. doi: 10.1016/j.molcel.2014.01.002.

Abstract

During X chromosome inactivation (XCI), the Polycomb Repressive Complex 2 (PRC2) is thought to participate in the early maintenance of the inactive state. Although Xist RNA is essential for the recruitment of PRC2 to the X chromosome, the precise mechanism remains unclear. Here, we demonstrate that the PRC2 cofactor Jarid2 is an important mediator of Xist-induced PRC2 targeting. The region containing the conserved B and F repeats of Xist is critical for Jarid2 recruitment via its unique N-terminal domain. Xist-induced Jarid2 recruitment occurs chromosome-wide independently of a functional PRC2 complex, unlike at other parts of the genome, such as CG-rich regions, where Jarid2 and PRC2 binding are interdependent. Conversely, we show that Jarid2 loss prevents efficient PRC2 and H3K27me3 enrichment to Xist-coated chromatin. Jarid2 thus represents an important intermediate between PRC2 and Xist RNA for the initial targeting of the PRC2 complex to the X chromosome during onset of XCI.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Dosage Compensation, Genetic
  • Humans
  • Mice
  • Polycomb Repressive Complex 2 / genetics
  • Polycomb Repressive Complex 2 / metabolism*
  • Polycomb Repressive Complex 2 / physiology
  • RNA, Long Noncoding / metabolism
  • RNA, Long Noncoding / physiology*
  • X Chromosome / metabolism*
  • X Chromosome Inactivation*

Substances

  • JARID2 protein, human
  • RNA, Long Noncoding
  • XIST non-coding RNA
  • Polycomb Repressive Complex 2

Associated data

  • GEO/GSE52073