Abstract
Randomly proliferating 3Y1stD123 cells are arrested in G1 phase within 24 h after a shift up to 39.8°C (temperature arrest), yet the density‐arrested cells (prepared at 33.8°C) enter S phase at 39.8°C with serum stimulation, with or without preexposure to 39.8°C for 24 h (Zaitsu and Kimura 1984a). When the density‐arrested 3Y1tsD123 cells were preexposed to 39.8°C for 96 h, they lost the ability to enter S phase at 39.8°C by serum stimulation and required a longer lag time to enter S phase at 33.8°C by serum stimulation than did the cells not preexposed to 39.8°C. Simian virus 40 induced cellular DNA synthesis at 39.8°C in the density‐arrested 3Y1tsD123 preexposed to 39.8°C for 96 h. In the absence of serum after a shift down to 33.8°C, the temperature‐arrested 3Y1stD123 cells entered S phase and then divided once. We postulate from these results that (1) that ts defect in 3Y1tsD123 is involved in a serum‐independent process. Once this process is accomplished, its accomplishment is invalidated slowly with preexposure to 39.8°C. This and the serum‐dependent processes occur in parallel but not necessarily simultaneously. The accomplishment of both (all) processes is required for the initiation of S phase. The density‐arrested 3Y1tsD123 cells have accomplished the serum‐independent process related to the ts defect, but have not accomplished serum‐dependent processes. In case of the temperature‐arrested 3Y1tsD123 cells, the reverse holds true. The lag time for entry into S phase depends on the preparedness for the initiation of DNA synthesis (on the extent of accomplishment of each of all processes required for entry into S phase). (2) To induce cellular DNA synthesis, simian virus 40 stimulates directly the serum‐independent process. However, we do not rule out the possibility that simian virus 40 stimulates serum‐dependent processes simultaneously.

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