A frameshift mutation affecting the carboxyl terminus of the simian virus 40 large tumor antigen results in a replication- and transformation-defective virus.
We have constructed a frameshift mutation in the simian virus 40 early region using a novel method of oligonucleotide-directed mutagenesis. The mutated DNA specifies an 84,000-dalton large tumor antigen that consists of approximately equal to 75,000 daltons encoded by the wild-type reading frame and 9,000 daltons, by the alternative reading frame (wild-type large tumor antigen is approximately equal to 82,000 daltons). The frameshifted carboxyl terminus of the protein bears a strong similarity to the same region of polyoma virus middle-sized tumor antigen. We have found that the mutant DNA is unable to replicate when introduced into permissive monkey cells and incapable of transforming nonpermissive mouse cells.
D000595:Amino Acid Sequence; D000818:Animals; D000957:Antigens, Viral, Tumor / Q000235:genetics*; D001483:Base Sequence; D002460:Cell Line; D002472:Cell Transformation, Viral; D002522:Chlorocebus aethiops; D004261:DNA Replication; D004262:DNA Restriction Enzymes; D007668:Kidney; D008970:Molecular Weight; D009154:Mutation; D010957:Plasmids; D013539:Simian virus 40 / Q000235:genetics* / Q000276:immunology; D014162:Transfection; D014779:Virus Replication
D000957:Antigens, Viral, Tumor; D004262:DNA Restriction Enzymes