Abstract
tsK -NRK rat cells infected with a temperature-sensitive mutant of the Kirsten murine sarcoma virus were arrested in the G 0 G 1 phase of their cell cycle by incubation in serum-deficient medium at a temperature (41°C) which inactivates the virus' abnormally thermolabile mitogenic/oncogenic 21 kDa (p 21) RAS protein product. Reactivating the viral RAS protein by lowering the temperature to a permissive 36°C rapidly (within 1 hour) stimulated adenylate cyclase, sensitized the enzyme to stimulation by GTP and forskolin and caused the tsK -NRK cells to transit G 1 and start replicating their DNA about 10 hours later. The 41°C → 36°C shift did not affect adenylate cyclase or stimulate G 1 transit in uninfected NRK cells. Thus, an oncogenic viral RAS protein was able to stimulate adenylate cyclase and G 1 transit in a mammalian cell just as other RAS proteins appear to do in yeast cells.
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