Chiarugi V, Porciatti F, Pasquali F, Magnelli L, Giannelli S, Ruggiero M
Laboratory of Molecular Biology, Istituto di Patologia Generale, Firenze, Italy.
Oncogene. 1987;2(1):37-40.
We have examined polyphosphoinositide turnover in a Rat-1 fibroblast line infected with a temperature-sensitive mutant (ts LA24) of the Rous sarcoma virus (RSV). When ts LA24-infected cells are shifted from the non-permissive to the permissive temperature, a rapid and sustained activation of phospholipase C (PLC) is observed. Normal and wild-type RSV-infected Rat-1 cells do not show any PLC activation upon temperature shiftdown. Pre-treatment of ts LA24-infected fibroblasts with tetrodotoxin (a Na+ channel inhibitor) or incubation in Na+-free medium significantly prevent temperature shiftdown-induced PLC activation. Therefore, we conclude that PLC activation occurs concomitantly with pp60v-src expression, and hypothesize that pp60v-src-related membrane depolarization is the causal link between pp60v-src tyrosine kinase activity and stimulation of polyphosphoinositide metabolism. Finally, we discuss the relationship between the phenomena we have observed and the mechanism of action of the ras oncogene.
我们检测了感染劳斯肉瘤病毒（RSV）温度敏感突变体（ts LA24）的大鼠-1成纤维细胞系中的多磷酸肌醇代谢转换。当感染ts LA24的细胞从非允许温度转移至允许温度时，可观察到磷脂酶C（PLC）迅速且持续的激活。正常和野生型RSV感染的大鼠-1细胞在温度下降时未显示任何PLC激活。用河豚毒素（一种Na+通道抑制剂）预处理感染ts LA24的成纤维细胞或在无Na+培养基中孵育可显著阻止温度下降诱导的PLC激活。因此，我们得出结论，PLC激活与pp60v-src表达同时发生，并推测与pp60v-src相关的膜去极化是pp60v-src酪氨酸激酶活性与多磷酸肌醇代谢刺激之间的因果联系。最后，我们讨论了我们观察到的现象与ras癌基因作用机制之间的关系。
