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 °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 °C were less than those at 39 °C. Pretreatment with PKC inhibitors, Ro-31- 85220 and staurosporine, enhanced the accumulation of IPt but not of PEt at 32 °C. The tyrosine phosphorylation of phospholipase Cγ1 (PLCγ1) was increased either by serum or by pp60(v-src) reactivation. These results suggest that serum transduces its signal through PLCγ1 mediation, and that pp60(v-src), possibly through the PKC mediation, negatively affects serum- induced PLCγ1 activation.