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


    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
    Issue number4
    Publication statusPublished - 15 Feb 2010


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


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