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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.

Original publication




Journal article


Genes & development

Publication Date





327 - 332


Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305, USA.


Cells, Cultured, Cell Line, Tumor, Chromatin, Animals, Humans, Mice, Caenorhabditis elegans, Neoplasms, Cell Differentiation, Cell Proliferation, Gene Expression Regulation, Methylation, Genome, Retinoblastoma Binding Proteins, Jumonji Domain-Containing Histone Demethylases