The histone demethylase UTX enables RB-dependent cell fate control

Jordon K. Wang, Miao Chih Tsai, Gino Poulin, Adam S. Adler, Shuzhen Chen, Helen Liu, Yang Shi, Howard Y. Chang

    Research output: Contribution to journalArticlepeer-review

    Abstract

    Trimethylation of histone H3 on Lys 27 (H3K27me3) is key for cell fate regulation. The H3K27me3 demethylase UTX functions in development and tumor suppression with undefined mechanisms. Here, genome-wide chromatin occupancy analysis of UTX and associated histone modifications reveals distinct classes of UTX target genes, including genes encoding Retinoblastoma (RB)-binding proteins. UTX removes H3K27me3 and maintains expression of several RB-binding proteins, enabling cell cycle arrest. Genetic interactions in mammalian cells and Caenorhabditis elegans show that UTX regulates cell fates via RB-dependent pathways. Thus, UTX defines an evolutionarily conserved mechanism to enable coordinate transcription of a RB network in cell fate control. © 2010 by Cold Spring Harbor Laboratory Press.
    Original languageEnglish
    Pages (from-to)327-332
    Number of pages5
    JournalGenes and development
    Volume24
    Issue number4
    DOIs
    Publication statusPublished - 15 Feb 2010

    Keywords

    • Cancer
    • Chromatin
    • Epigenetics
    • Gene regulation
    • Histone demethylation

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