trans-dominant defective mutants of simian virus 40 T antigen.
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.
D000595:Amino Acid Sequence; D000818:Animals; D000952:Antigens, Polyomavirus Transforming; D000957:Antigens, Viral, Tumor / Q000235:genetics*; D001483:Base Sequence; D002460:Cell Line; D002471:Cell Transformation, Neoplastic; D004261:DNA Replication; D003673:Defective Viruses / Q000201:enzymology / Q000235:genetics*; D005796:Genes; D005799:Genes, Dominant; D005814:Genes, Viral; D009154:Mutation; D009856:Oncogene Proteins, Viral / Q000235:genetics*; D010957:Plasmids; D011494:Protein Kinases / Q000235:genetics*; D051381:Rats; D013539:Simian virus 40 / Q000201:enzymology / Q000235:genetics*
D000952:Antigens, Polyomavirus Transforming; D000957:Antigens, Viral, Tumor; D009856:Oncogene Proteins, Viral; D011494:Protein Kinases