Role of src gene in growth regulation of Rous sarcoma virus-infected chicken embryo fibroblasts

Abstract

We report here a study of the mechanisms leading to loss of growth control in chicken embryo fibroblasts transformed by Rous sarcoma virus (RSV). We have been particularly concerned with the role of the src gene in this process, and have used RSV mutants temperature sensitive (ts) for transformation to investigate the nature of the growth regulatory lesion. The two principal findings were (1) the stationary phase of the cell cycle (G₁) in chick embryo fibroblasts seems to have two distinct regulatory compartments (using the terminology of Brooks et al.¹ we refer to these as ‘Q’ and ‘A’ states). When rendered stationary at 41.5 °C by serum deprivation, normal cells enter a Q state, but cells infected with the ts-mutant occupy an A state. (2) Whereas normal cells can occupy either state depending on culture conditions, the ts-infected cells, at 41.5 °C, do not seem to enter Q even though a known src gene product, a kinase, is reported to be inactive at this temperature^2,3. We discuss the possibility that viral factors other than the active src protein kinase influence growth control in infected cultures.