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Tip60-dependent acetylation of p53 modulates the decision between cell-cycle arrest and apoptosis

Yi Tang1, Jianyuan Luo, Wenzhu Zhang

  • 1Institute for Cancer Genetics, Surgeons, Columbia University, 1150 St. Nicholas Ave, New York, New York 10032, USA.

Molecular Cell
|December 26, 2006
PubMed

Insights

The protein Tip60 acetylates p53 at K120, a modification crucial for p53-mediated apoptosis but not cell growth arrest. This acetylation regulates the cell

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The tumor suppressor protein p53 plays a critical role in cellular response to DNA damage.
  • p53 can induce either cell-cycle arrest or apoptosis, but the mechanisms governing this choice are unclear.

Purpose of the Study:

  • To investigate the role of Tip60 in p53-mediated cellular responses.
  • To identify the specific posttranslational modification of p53 by Tip60 and its functional significance.

Main Methods:

  • Investigated the interaction between Tip60 and p53.
  • Analyzed p53 acetylation at specific lysine residues, particularly K120.
  • Utilized acetylation-defective p53 mutants (K120R) to assess functional outcomes.
  • Examined p53-mediated apoptosis and cell-cycle arrest.

Main Results:

  • Tip60 is essential for both p53-mediated cell growth arrest and apoptosis.
  • Tip60 specifically acetylates p53 at lysine 120 (K120) within the DNA-binding domain.
  • Acetylation at K120 is critical for p53-dependent apoptosis but not for growth arrest.
  • A cancer-associated p53 mutant (K120R) failed to induce apoptosis but retained growth arrest function.

Conclusions:

  • Tip60-dependent acetylation of p53 at K120 is a key regulator determining the cell fate decision between apoptosis and cell-cycle arrest.
  • The DNA-binding core domain of p53 is a critical target for posttranslational modifications that modulate its function.
  • Understanding this regulatory mechanism provides insights into cancer development and potential therapeutic strategies.

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