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PMID: 6285001 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Mutant of simian virus 40 large T-antigen that is defective for viral DNA synthesis, but competent for transformation of cultured rat cells.

Journal of virology ·Vol. 42 ·No. 3 ·1982-06-00 ·Pages 854-64

Stringer JR

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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31 references, click to expand
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Article Info
Journal
Journal of virology
Abbr.
J Virol
ISSN
0022-538X
Published
1982-06-00
Pages
854-64
Language
English
Region
United States
NLM ID
0113724
PMCID
PMC256919
Subset
IM
Grants
NCI NIH HHS · CA-06460 · United States
NCI NIH HHS · CA-13106 · United States
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