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).

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http://dx.doi.org/10.1007/BF01871631DOI Listing

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