Abstract
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.
MeSH Terms
Animals
Antigens, Viral/genetics
Antigens, Viral, Tumor
Base Sequence
Cell Line
Cell Transformation, Viral
DNA Replication
DNA, Viral/biosynthesis,genetics
Genes, Viral
Mutation
Simian virus 40/genetics,immunology
Chemicals
Antigens, Viral
Antigens, Viral, Tumor
DNA, Viral
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Stringer J R
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