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 language | English |
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Pages (from-to) | 327-332 |
Number of pages | 5 |
Journal | Genes and development |
Volume | 24 |
Issue number | 4 |
DOIs | |
Publication status | Published - 15 Feb 2010 |
Keywords
- Cancer
- Chromatin
- Epigenetics
- Gene regulation
- Histone demethylation