Abstract
NRK cells infected with a temperature‐sensitive, transformation‐defective mutant of avian sarcoma virus (ASV), __ts__LA23, behaved as if nontransformed at a nonpermissive 40°C and were rendered quiescent by serum deprivation. These serum‐deprived cells were stimulated to start entering S phase about 7 hours after serum addition at 40°C or about 9 hours after shifting the cultures to 36°C, a temperature allowing the production of active viral pp60^src^ and expression of the transformed phenotype. The transit of both serum‐and temperature‐stimulated __ts__LA23‐NRK cells through later G~1~ was inhibited by the unrelated calmodulin antagonists W7 and R24571. The former drug was found to block the cells at a point in the cell cycle no more than 2 hours from the G~1~/S transition. The weaker calmodulin antagonist, W5, was less effective in impairing progression. Thus, calmodulin is likely required for the transit of both transformed and phenotypically normal __ts__LA23‐NRK cells through the later stages of their G~1~ phases. Cells neoplastically transformed by ASV contain more calmodulin than uninfected, non‐neoplastic cells. At the nonpermissive 40°C, the calmodulin content of the __ts__LA23‐NRK cells dropped to the non‐neoplastic level. When these phenotypically non‐transformed cells were enabled to reenter the cell cycle while still in low‐serum medium by a 40 to 36°C shift, they passed through the G~1~ and S phases and divided without a concomitant rise in the total calmodulin content. Thus, a calmodulin rise does not appear to be required for the expression of one characteristic of transformed cells, i.e., reduced requirement for exogenous growth factors.