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Cell-specific modulation of papovavirus replication by tumor suppressor protein p53

D Lepik1, M Ustav

  • 1Department of Microbiology and Virology, Institute of Molecular and Cell Biology, Tartu University and Estonian Biocentre, Tartu EE2400, Estonia.

Journal of Virology
|April 25, 2000
PubMed

Insights

Mouse polyomavirus (Py) replication is not suppressed by the p53 protein in mouse cells, unlike in hamster or human cells. This suggests p53 is inactive in suppressing papovavirus replication specifically in mouse cells.

Area of Science:

  • Molecular Biology
  • Virology
  • Cell Cycle Regulation

Background:

  • Small DNA tumor viruses modulate cellular tumor suppressor proteins p53 and pRB for replication.
  • Inactivation of p53 and pRB is thought to direct cells into the S phase for viral replication.
  • Mouse polyomavirus (Py) modulates pRB but not p53 activity.

Purpose of the Study:

  • To investigate the role of p53 in suppressing Py and papillomavirus replication in mouse cells compared to other species.
  • To determine if p53's tumor suppressor activity is species-specific regarding papovavirus replication.

Main Methods:

  • Replication assays of Py and papillomavirus origins in various cell lines (mouse, hamster, human).
  • Analysis of p53's effect on viral replication in different species.
  • Deletion analysis of p53 protein domains to identify functional regions for replication suppression.

Main Results:

  • Py replication and papillomavirus origin replication were insensitive to p53 in mouse cells.
  • Replication of both Py and papillomavirus origins was efficiently blocked by p53 in hamster and human cells.
  • Specific p53 domains (RPA binding, proline-rich, DNA-binding, oligomerization) are necessary for its suppressive function.

Conclusions:

  • The p53 protein's ability to suppress papovavirus replication is species-specific, being inactive in mouse cells.
  • This inactivity of p53 in mouse cells may facilitate papovavirus replication in this host.
  • Understanding these species-specific interactions is crucial for viral pathogenesis research.

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