The histone demethylase UTX enables RB-dependent cell fate control.
Genes Dev, 2010/2/15;24(4):327-32.
Wang JK[1], Tsai MC, Poulin G, Adler AS, Chen S, Liu H, Shi Y, Chang HY
Affiliations
PMID: 20123895DOI: 10.1101/gad.1882610
Impact factor: 12.89
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.
MeSH terms
Animals; Caenorhabditis elegans; Cell Differentiation; Cell Line, Tumor; Cell Proliferation; Cells, Cultured; Chromatin; Gene Expression Regulation; Genome; Humans; Jumonji Domain-Containing Histone Demethylases; Methylation; Mice; Neoplasms; Retinoblastoma Binding Proteins
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