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PMID: 6312452 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Intracistronic complementation in the simian virus 40 A gene.

Tornow J, Cole CN

Abstract

A set of eight simian virus 40 mutants was constructed with lesions in the A gene, which encodes the large tumor (T) antigen. These mutants have small deletions (3-20 base pairs) at either 0.497, 0.288, or 0.243 map units. Mutants having both in-phase and frameshift mutations at each site were isolated. Neither plaque formation nor replication of the mutant DNAs could be detected after transfection of monkey kidney cells. Another nonviable mutant, dlA2459, had a 14-base-pair deletion at 0.193 map unit and was positive for viral DNA replication. Each of the eight mutants were tested for ability to form plaques after cotransfection with dlA2459 DNA. The four mutants that had in-phase deletions were able to complement dlA2459. The other four, which had frameshift deletions, did not. No plaques were formed after cotransfection of cells with any other pair of group A mutants. This suggests that the defect in dlA2459 defines a distinct functional domain of simian virus 40 T antigen.

MeSH Terms
Antigens, Viral, Tumor/genetics Chromosome Deletion DNA Replication DNA, Viral/genetics Genes, Viral Genetic Complementation Test Mutation Simian virus 40/genetics
Chemicals
Antigens, Viral, Tumor DNA, Viral
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Tornow J
Cole C N
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39 references, click to expand
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Article Info
Journal
Proceedings of the National Academy of Sciences of the United States of America
Abbr.
Proc Natl Acad Sci U S A
ISSN
0027-8424
Published
1983-10-00
Pages
6312-6
Language
English
Region
United States
NLM ID
7505876
PMCID
PMC394287
Subset
IM
Databases
GENBANK
J02400, J02402, J02403, J02406, J02407, J02408, J02409, J02410, V01380
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