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The histone demethylase UTX enables RB-dependent cell fate control.

Genes & development | Feb 15, 2010

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.

Pubmed ID: 20123895 RIS Download

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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Associated grants

  • Agency: NCI NIH HHS, Id: R01-CA118487
  • Agency: Medical Research Council, Id: G0600127
  • Agency: NCI NIH HHS, Id: R01 CA118487
  • Agency: Howard Hughes Medical Institute, Id: R01-CA118750
  • Agency: NCI NIH HHS, Id: R01 CA118750
  • Agency: NCI NIH HHS, Id:

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