Mutant of simian virus 40 large T-antigen that is defective for viral DNA synthesis, but competent for transformation of cultured rat cells.
A mutant was isolated which demonstrates that the transforming activity of simian virus 40 large T-antigen is separable from its function in viral DNA replication. The mutant, SVR9D, is nonconditionally defective for viral DNA synthesis, but competent at wild-type level for morphological transformation of cultured rat cells. The lytic growth defect in SVR9D is complemented by the simian virus 40 A gene product present in the transformed CV1 cell line, COS1. The lesion in SVR9D DNA was mapped genetically by marker rescue of plaque formation and localized to a 214-base-pair segment of the viral genome bounded by nucleotide numbers 4100 and 4314. DNA sequence analysis showed the mutation to be an adenine-to-guanine transition at nucleotide number 4178. This change predicts a lysine-to-glutamic acid amino acid change at residue number 214 of the mutant large T-antigen polypeptide.
D000818:Animals; D000956:Antigens, Viral / Q000235:genetics*; D000957:Antigens, Viral, Tumor; D001483:Base Sequence; D002460:Cell Line; D002472:Cell Transformation, Viral; D004261:DNA Replication; D004279:DNA, Viral / Q000096:biosynthesis* / Q000235:genetics; D005814:Genes, Viral; D009154:Mutation; D013539:Simian virus 40 / Q000235:genetics / Q000276:immunology*
D000956:Antigens, Viral; D000957:Antigens, Viral, Tumor; D004279:DNA, Viral