p53-dependent transcription and tumor suppression are not affected in Set7/9-deficient mice

Mol Cell. 2011 Aug 19;43(4):673-80. doi: 10.1016/j.molcel.2011.08.006.

Abstract

Methylation of specific lysine residues in the C terminus of p53 is thought to govern p53-dependent transcription following genotoxic and oncogenic stress. In particular, Set7/9 (KMT7)-mediated monomethylation of human p53 at lysine 372 (p53K372me1) was suggested to be essential for p53 activation in human cell lines. This finding was confirmed in a Set7/9 knockout mouse model (Kurash et al., 2008). In an independent knockout mouse strain deficient in Set7/9, we have investigated its involvement in p53 regulation and find that cells from these mice are normal in their ability to induce p53-dependent transcription following genotoxic and oncogenic insults. Most importantly, we detect no impairment in canonical p53 functions in these mice, indicating that Set7/9-mediated methylation of p53 does not seem to represent a major regulatory event and does not appreciably control p53 activity in vivo.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Cell Cycle
  • Cellular Senescence / genetics
  • Gene Expression Regulation
  • Mice
  • Mice, Inbred C57BL
  • Protein Methyltransferases / genetics*
  • Protein Methyltransferases / metabolism
  • Protein Methyltransferases / physiology
  • Transcription, Genetic*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • Tumor Suppressor Protein p53 / physiology*

Substances

  • Tumor Suppressor Protein p53
  • Protein Methyltransferases
  • Setd7 protein, mouse