Pp60v-src reactivation inhibits serum-induced accumulation of inositol phosphates and phosphatidylethanol in tsNRK.

Abstract

In tsRSV-infected NRK (tsNRK) cells, pp60(v-src) reactivation by temperature-shift from a nonpermissive temperature, 39 C, to a permissive one, 32 degrees C, induced the production of inositol phosphates (IPt) and phosphatidylethanol (PEt). This was accompanied by an increase in membrane-associated protein kinase C (PKC) activity in the absence of exogenous growth factors. However, with serum-stimulation, the amounts of IPt and PEt at 32 degrees C were less than those at 39 degrees C. Pretreatment with PKC inhibitors, Ro-31-8220 and staurosporine, enhanced the accumulation of IPt but not of PEt at 32 degrees C. The tyrosine phosphorylation of phospholipase Cgamma1 (PLCgamma1) was increased either by serum or by pp60(v-src) reactivation. These results suggest that serum transduces its signal through PLCgamma1 mediation, and that pp60(v-src), possibly through the PKC mediation, negatively affects serum-induced PLCgamma1 activation.