-NRK rat cells infected with a temperature-sensitive mutant of the Kirsten murine sarcoma virus were arrested in the G₀/G₁ 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 -NRK cells to transit G₁ and start replicating their DNA about 10 hours later. The 41°C → 36°C shift did not affect adenylate cyclase or stimulate G₁ transit in uninfected NRK cells. Thus, an oncogenic viral RAS protein was able to stimulate adenylate cyclase and G₁ transit in a mammalian cell just as other RAS proteins appear to do in yeast cells.