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. 1987 Feb;61(2):436–445. doi: 10.1128/jvi.61.2.436-445.1987

trans-dominant defective mutants of simian virus 40 T antigen.

J M Farber, K W Peden, D Nathans
PMCID: PMC253967  PMID: 3027373

Abstract

We constructed a collection of linker insertion mutants in the simian virus 40 (SV40) genome and studied several of these with changes limited to a part of the large T antigen gene corresponding to an amino acid sequence shared with other ATPases. Two of these mutants were found to have a novel phenotype in that they could not be complemented for plaque formation by a late-region deletion mutant. These two mutants, in contrast to other mutants in this region, were able to transform rat cells in culture at a frequency close to that of the wild-type gene. The noncomplementing mutants were found to be potent inhibitors of SV40 DNA replication despite the presence of wild-type T antigen in the transfected cells. This inhibition was shown to be the result of the introduced mutations in the large T antigen gene. We conclude that the large T antigens of the noncomplementing mutants can act as inhibitors of SV40 DNA replication.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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