Functional rescue of temperature-sensitive defects in the cell-cycle mutants of rat 3Y1 fibroblasts by the small t-antigen deletion mutant of simian virus 40

Cell Struct Funct. 1989 Aug;14(4):375-82. doi: 10.1247/csf.14.375.

Abstract

We examined the effects of large T antigen of simian virus 40 (SV40) on the proliferation phenotypes of temperature-sensitive (ts) mutants of rat 3Y1 fibroblasts, which cease proliferating in the G1 phase of the cell cycle at a restrictive temperature (39.8 degrees C). Four ts mutants, each representing independent complementation groups, were transformed with the dl-884 mutant of SV40 which lacks the unique coding region for small t antigen. In the case of two ts mutants, their transformed derivatives did not cease proliferation at 39.8 degrees C. In the other two mutants, the transformed cells continued to enter the S phase but the cells became detached from the dishes thereafter, at 39.8 degrees C. The proliferation phenotypes of the dl-884-transformed cells at 39.8 degrees C were quite similar with those of the same mutants transformed with the wild-type SV40. These results indicate that large T antigen alone is sufficient to overcome the inhibition of cellular entry into S phase caused by four different ts defects and determines the proliferation phenotypes of the cells after entering the S phase at a restrictive temperature, and that small t antigen does not alter the cellular phenotypes determined by large T antigen.

MeSH terms

  • Animals
  • Antigens, Polyomavirus Transforming / genetics*
  • Cell Cycle
  • Cell Division
  • Cell Line
  • Chromosome Deletion
  • Fibroblasts / cytology*
  • Fibroblasts / physiology
  • Mutation
  • Phenotype
  • Rats
  • Rats, Mutant Strains
  • Simian virus 40 / immunology*
  • Temperature*

Substances

  • Antigens, Polyomavirus Transforming