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p53 targets simian virus 40 large T antigen for acetylation by CBP

Danielle L Poulin1, Andrew L Kung, James A DeCaprio

  • 1Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA.

Journal of Virology
|July 16, 2004
PubMed

Insights

Simian virus 40 (SV40) large T antigen acetylation depends on p53 and CBP. This acetylation, occurring at lysine 697, is conserved in related human polyomavirus T antigens, suggesting a shared regulatory mechanism.

Area of Science:

  • Virology
  • Molecular Biology
  • Cancer Research

Background:

  • Simian virus 40 (SV40) large T antigen (T Ag) interacts with tumor suppressor p53 and coactivators CBP/p300.
  • This interaction is crucial for T Ag-mediated cellular transformation.
  • CBP/p300's modulation of p53 function is linked to cell proliferation and tumorigenesis regulation.

Purpose of the Study:

  • To investigate the role of CBP/p300 in SV40 T Ag function.
  • To explore the interplay between p53, CBP, and SV40 T Ag acetylation.
  • To identify the specific acetylation site on T Ag and its conservation.

Main Methods:

  • In vivo acetylation assays of SV40 T Ag.
  • Analysis of T Ag acetylation dependence on p53 and CBP.
  • Mapping of the T Ag acetylation site.
  • Comparative analysis of T antigens from human polyomaviruses JC and BK.

Main Results:

  • SV40 T Ag is acetylated in vivo in a p53-dependent manner, primarily mediated by CBP.
  • T Ag acetylation requires the interaction between T Ag and p53, and between p53 and CBP.
  • Acetylation occurs at C-terminal lysine residue 697 of T Ag.
  • Corresponding acetylation sites were found in JC and BK T antigens.

Conclusions:

  • CBP-mediated acetylation of SV40 T Ag is dependent on p53.
  • This p53-dependent acetylation mechanism is conserved among human polyomavirus T antigens.
  • T Ag acetylation may regulate T Ag binding or other functions.

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