期刊
MOLECULAR CELL
卷 53, 期 2, 页码 301-316出版社
CELL PRESS
DOI: 10.1016/j.molcel.2014.01.002
关键词
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资金
- Marie Curie Fellowship [237675 FP7-People-IEF-2008]
- Ligue Nationale contre le cancer
- EpiGeneSys FP7, Network of Excellence [257082]
- ERC Advanced Investigator award [250367]
- EU FP7 SYBOSS grant [242129]
- Labex DEEP
- ATIP-Avenir program
- Fondation pour la Recherche Medicale (FRM)
- European Research Council (ERC-Stg)
- Curie Institute
- Agence Nationale de le Recherche (investissements d'avenir) [ANR-10-EQPX-03, ANR10-INBS-09-08]
- Canceropole Ile-de-France
- European Research Council (ERC) [250367] Funding Source: European Research Council (ERC)
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.
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