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

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


  • Wang JK
  • Tsai MC
  • Poulin G
  • Adler AS
  • Chen S
  • Liu H
  • Shi Y
  • Chang HY


Genes & development

Publication Data

February 15, 2010

Associated Grants

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

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