We investigated the relationship in between the cell cycle start function, and two mutants defining components of the cAMP pathway. The thermolabile adenylate cyclase mutant (ts) is phenotypically similar to the temperature-sensitive mutant (ts) in that both mutants, when shifted to the restrictive temperature, arrest in G1 of the cell cycle and permit the initiation of meiosis and sporulation. The mutant [a lesion resulting in a low level of regulatory (R) subunit and a high level of active, catalytic (C) subunit of the CAMP-dependent protein kinase] suppresses the temperature-sensitive phenotype of (ts) and confers an asporogenous phenotype. We found that (ts) complemented (ts), and, unlike (ts), was not suppressible by demonstrating that and must encode different functions. Also our results indicate that does not encode the R subunit of the CAMP-dependent protein kinase. In addition, although the (ts) double mutant was temperature sensitive like (ts), we found that the (ts) homozygous diploid was asporogenous like The inability of the (ts) double mutant to sporulate demonstrated that does not encode the C subunit of the cAMP kinase, and indicated that the function modulates the cAMP pathway to control meiosis and sporulation. Further, the temperature-sensitive phenotype of the double mutant, and hence the inability of to suppress (ts), suggested that a second cell cycle function exists which is independent of the cAMP pathway. Taken together, our genetic data indicated that the protein has a dual regulatory role: (1) to control the decision between proliferation and differentiation by controlling the cAMP pathway; and (2) to control the cell cycle positively by a mechanism independent of the cAMP pathway. (ts) and