Abstract
We studied the action of temperature-sensitive mutant simian virus 40--a transformation-inducing DNA virus--on the junctional permeability to mono-, di- and triglutamate in rat embryo-, pancreas islet (epithelial)-, and 10T1/2 cell cultures. Junctional permeability was reduced (reversibly) in the transformed state. To dissect the genetics of this alteration, we used two kinds of mutant virus DNA. One kind had a temperature-sensitive mutation on the A gene, rendering the large T antigen (the gene product) thermolabile (T+ in equilibrium T-). The other had a deletion on the F gene, in addition, abolishing (permanently) the expression of the little t addition (t-). The junctional alteration occurred in the condition T+ t+, but not in the conditions T- t+, T+ t- or T- t-. Both antigens, thus, are necessary for this junctional alteration--a genetic requirement identical to that for decontrol of growth (but distinct from that of the cytoskeletal alteration).
MeSH Terms
Animals
Antigens, Viral, Tumor
Cell Communication
Cell Division
Cell Transformation, Viral
Cells, Cultured
Intercellular Junctions/physiology
Islets of Langerhans
Rats
Simian virus 40
Viral Proteins/physiology
Chemicals
Antigens, Viral, Tumor
Viral Proteins
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Azarnia R
Loewenstein W R
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29 references, click to expand
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