Summary
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 (epithelia)-, 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 theA gene, rendering the largeT antigen (the gene product) thermolabile (T + ⇆T −). The other had a deletion on theF gene, in addition, abolishing (permanently) the expression of the littlet antigen (t −). The junctional alteration occurred in the conditionT + t +, but not in the conditionsT − t +,T + t − orT − 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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Azarnia, R., Loewenstein, W.R. Intercellular communication and the control of growth: XII. Alteration of junctional permeability by simian virus 40. roles of the large and smallT antigens. J. Membrain Biol. 82, 213–220 (1984). https://doi.org/10.1007/BF01871631
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DOI: https://doi.org/10.1007/BF01871631