Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

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

DOI

10.1101/gad.1882610

Type

Journal article

Journal

Genes & development

Publication Date

02/2010

Volume

24

Pages

327 - 332

Addresses

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

Keywords

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