SPECIFIC ACTIVATION OF PHOSPHATIDYLCHOLINE TURNOVER IN HAMSTER FIBROBLASTS TRANSFORMED BY THE ROUS-SARCOMA VIRUS

Transformation of hamster embryonic fibroblasts by the Rous sarcoma vi rus caused a sharp increase in the turnover of phosphatidylcholine, a cellular phospholipid. A decrease in the growth rate of the Rous-sarco ma-virus-transformed cells (HETSR strain) is accompanied by an additio nal activation of phosphatidylcholine metabolism during monolayer form ation. A similar effect is observed after prolonged culturing of the c ells in the presence of dexamethasone. Addition of the tyrosine kinase inhibitor genistein selectively inhibits phosphatidylcholine synthesi s without affecting the synthesis of phosphoinositides. Immunoblotting analysis of the p60-src protein (a product of the v-src viral oncogen e of the tyrosine kinase family) failed to reveal significant changes in the synthesis and activity of this protein during the dexamethasone -induced inhibition of HETSR cell growth. These results suggest select ive activation of phosphatidylcholine metabolism in the src-transforme d cells increasing with the decrease in the cell growth rate. The p60- src synthesis does not depend on dexamethasone, and its presence in th e HETSR cells is suggested to be one of the factors responsible for th e increased level of phosphatidylcholine metabolism, thereby promoting cell growth under the limited activity of growth substances.