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Mouse p53 blocks SV40 DNA replication in vitro and downregulates T antigen DNA helicase activity

H W Stürzbecher1, R Brain, T Maimets

  • 1Cell Proliferation Laboratory, Marie Curie Research Institute, Oxted, Surrey, UK.

Oncogene
|October 1, 1988
PubMed

Insights

Mouse p53 protein suppresses simian virus 40 (SV40) DNA replication by directly inhibiting T-antigen helicase activity. This p53 function occurs in vivo and in cell extracts, impacting DNA synthesis but not transcription.

Area of Science:

  • Molecular Biology
  • Virology
  • Biochemistry

Background:

  • The tumor suppressor protein p53 plays a critical role in cellular processes, including DNA replication and transcription.
  • Simian virus 40 (SV40) replication is a well-studied model system involving the viral T-antigen.
  • Understanding the interaction between p53 and viral replication machinery is crucial for deciphering cellular defense mechanisms.

Purpose of the Study:

  • To investigate the mechanism by which non-primate p53 suppresses SV40 DNA replication.
  • To determine if mouse p53 affects T-antigen's DNA replication or transcription functions.

Main Methods:

  • Utilized immunopurified mouse p53 proteins in HeLa cell extracts.
  • Assessed the impact of mouse p53 on T-antigen dependent DNA synthesis and SV40 early transcription.
  • Evaluated T-antigen's ATPase, DNA binding, and helicase activities in the presence of mouse p53.

Main Results:

  • Mouse p53 inhibited T-antigen dependent DNA synthesis in replication-competent HeLa cell extracts.
  • Mouse p53 did not affect SV40 early transcription or T-antigen's ability to downregulate it.
  • Mouse p53 showed no significant impact on T-antigen's ATPase and DNA binding activities but moderately reduced helicase activity.

Conclusions:

  • Mouse p53 directly modulates T-antigen function, specifically reducing its helicase activity.
  • This modulation of T-antigen helicase activity is a key mechanism for the in vivo suppression of SV40 replication by mouse p53.

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