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Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
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The methyltransferase Set7/9 (Setd7) is dispensable for the p53-mediated DNA damage response in vivo

Stefano Campaner1, Fabio Spreafico, Thomas Burgold

  • 1Department of Experimental Oncology, European Institute of Oncology at the IFOM-IEO-Campus, Via Adamello 16, 20139 Milan, Italy.

Molecular Cell
|August 23, 2011
PubMed

Insights

The enzyme Set7/9 (also called Setd7) is not essential for p53 protein function in mice. Our study found Set7/9 is dispensable for p53-mediated cell cycle arrest and apoptosis following DNA damage.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • p53 is a crucial regulator of cell fate in response to DNA damage and oncogene activation.
  • Posttranslational modifications, including lysine methylation by Set7/9 (Setd7), control p53 activity.
  • Previous studies suggested Set7/9-mediated methylation promotes p53 acetylation, stabilization, and activation in human cells.

Purpose of the Study:

  • To investigate the physiological relevance of Set7/9-mediated p53 regulation in vivo.
  • To determine if Set7/9 is essential for p53-dependent responses in mice.

Main Methods:

  • Utilized an independent Set7/9 knockout mouse strain.
  • Assessed p53-dependent cell-cycle arrest and apoptosis following DNA damage (radiation, genotoxic agents).
  • Analyzed p53 acetylation, c-myc oncogene-induced apoptosis, and p53 target gene expression.

Main Results:

  • Deletion of Set7/9 did not affect p53-dependent cell-cycle arrest or apoptosis after DNA damage.
  • Set7/9 was not required for p53 acetylation following irradiation.
  • p53-mediated apoptosis induced by c-myc oncogene was independent of Set7/9.
  • Set7/9 dispensable for p53-dependent gene expression program.

Conclusions:

  • Set7/9 is dispensable for p53 function in mice.
  • The proposed role of Set7/9 in promoting p53 acetylation, stabilization, and activation in vivo is not supported by our findings.

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