Simian virus 40 compensates a cellular mutational defect of a serum-dependent function controlling cell cycle progression in the G2 phase.

Rat 3Y1tsF121 fibroblasts are arrested in the G2 phase at the nonpermissive temperature due to a temperature-sensitive (ts) defect, and the G2 arrest is overcome at the nonpermissive temperature by the addition of a large dose of fresh serum. When the G2-arrested cells which had been exposed to the nonpermissive temperature for 12 hr were shifted down to the permissive temperature, most divided within 12 hr. When the cultures prepared in parallel were infected with simian virus 40 (SV40) at the nonpermissive temperature, the G2-arrested cells divided as early as 6 hr after the expression of T antigen. The G2-arrested cells, which had been exposed to the nonpermissive temperature for 36 hr, lost both the ability to restore the G2 and M traverse at the nonpermissive temperature after the addition of fresh serum and the reversibility of the arrest upon shift down to the permissive temperature. However, SV40 induced these cells to divide at the nonpermissive temperature, as in the case of the reversibly arrested cells. A small t-antigen-deletion mutant (dl-884) also induced both types of the G2-arrested cells to divide at the nonpermissive temperature. These results suggest that (1) SV40 compensates or activates, in the G2 phase, the function regulating G2 and M transition by serum; (2) SV40 induces restoration of the irreversible G2 arrest; and (3) small t antigen is not responsible for these activities of SV40.