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SUZ12 is required for both the histone methyltransferase activity and the silencing function of the EED-EZH2 complex.

Recent studies have revealed the intrinsic histone methyltransferase (HMTase) activity of the EED-EZH2 complex and its role in Hox gene silencing, X inactivation, and cancer metastasis. In this study, we focus on the function of individual components. We found that the HMTase activity requires a minimum of three components-EZH2, EED, and SUZ12-while AEBP2 is required for optimal enzymatic activity. Using a stable SUZ12 knockdown cell line, we show SUZ12 knockdown results in cell growth defects, which correlate with genome-wide alteration on H3-K27 methylation as well as upregulation of a number of Hox genes. Chromatin immunoprecipitation (ChIP) assay identified a 500 bp region located 4 kb upstream of the HoxA9 transcription initiation site as a SUZ12 binding site, which responds to SUZ12 knockdown and might play an important role in regulating HoxA9 expression. Thus, our study establishes a critical role of SUZ12 in H3-lysine 27 methylation and Hox gene silencing.

Pubmed ID: 15225548

Authors

  • Cao R
  • Zhang Y

Journal

Molecular cell

Publication Data

July 2, 2004

Associated Grants

  • Agency: NIGMS NIH HHS, Id: GM68804

Mesh Terms

  • Binding Sites
  • Cell Division
  • DNA-Binding Proteins
  • Gene Expression Regulation, Developmental
  • Gene Silencing
  • Gene Targeting
  • Genes, Homeobox
  • HeLa Cells
  • Histone-Lysine N-Methyltransferase
  • Histones
  • Homeodomain Proteins
  • Humans
  • Lysine
  • Methylation
  • Mutation
  • Neoplasm Proteins
  • Polycomb Repressive Complex 2
  • Protein Methyltransferases
  • Proteins
  • Repressor Proteins
  • Silencer Elements, Transcriptional
  • Transcription Factors
  • Up-Regulation