Reversion of transformed glycolysis to normal by inhibition of protein synthesis in rat kidney cells infected with temperature-sensitive mutant of Rous sarcoma virus.

Abstract

Normal rat kidney cells infected with a temperature-sensitive mutant (LA23) of Rous sarcoma virus exhibit the transformed phenotype when grown at 33.degree. C and the normal phenotype at 39.degree. C. The addition of protein synthesis inhibitors to LA23-infected cells grown at 33.degree. C causes them to revert, over a 12-h period, to the normal phenotype with respect to morphological and cytoskeletal characteristics. Reversion of the metabolic characteristics of the transformed phenotype to those of the normal also occurs under these conditions. LA23-Infected cells show an increased rate of aerobic glycolysis at 33.degree. C compared to that at 39.degree. C. They also show a different sensitivity of that rate to dinitrophenol and oligomycin at 33.degree. C compared to 39.degree. C. Such cells grown at 33.degree. C in the presence of cycloheximide or abrin rapidly recover the aerobic glycolysis characteristics of the normal phenotype. Apparently, transformation by the src gene of the Rous sarcoma virus is a pleiotypic and reversible process, such as is involved in a pleiotypic enzymic modification reaction and its reversal.