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Targeting of p300/CREB binding protein coactivators by simian virus 40 is mediated through p53

Darrell R Borger1, James A DeCaprio

  • 1Dana-Farber Cancer Institute, Department of Medical Oncology, Harvard Medical School, Mayer Building 457, 44 Binney Street, Boston, Massachusetts 02115, USA.

Journal of Virology
|April 14, 2006
PubMed

Insights

Simian virus 40 large T antigen (SV40 LT) utilizes p53 to bind CBP/p300 coactivators. This interaction modifies SV40 LT, leading to its acetylation.

Area of Science:

  • Molecular Biology
  • Virology
  • Cancer Research

Background:

  • Simian virus 40 large T antigen (SV40 LT) is known to inactivate tumor suppressors p53 and retinoblastoma proteins.
  • p53 normally interacts with CBP/p300 coactivators, forming a ternary complex with SV40 LT.

Purpose of the Study:

  • To investigate the secondary role of p53 in mediating the interaction between SV40 LT and CBP/p300 coactivators.
  • To elucidate the post-translational modifications of p53 and SV40 LT within this complex.

Main Methods:

  • Analysis of post-translational modifications of p53 associated with SV40 LT.
  • Assessment of p53 phosphorylation at S15 upon SV40 LT expression.
  • Reconstitution of the SV40 LT-CBP/p300 complex in p53-null cells.
  • RNA interference to deplete endogenous p53 and observe complex disruption.
  • Investigation of SV40 LT acetylation dependent on p300 and p53.

Main Results:

  • p53 bound to SV40 LT undergoes post-translational modifications indicative of CBP/p300 binding.
  • SV40 LT expression increases p53 phosphorylation at S15.
  • p53 is essential for bridging SV40 LT and CBP/p300, as demonstrated by complex reconstitution and disruption experiments.
  • SV40 LT acetylation by p300 is dependent on p53, involving the CH3 domain of p300.

Conclusions:

  • p53 acts as a crucial bridge, facilitating the interaction between SV40 LT and CBP/p300 coactivators.
  • The binding of p53 to SV40 LT targets CBP/p300 for the acetylation of SV40 LT, a novel modification pathway.

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