In the yeast Saccharomyces cerevisiae, addition of glucose to cells grown under glucose-derepressed conditions induces a transient rise in the intracellular level of cAMP. This modulation requires functional elements of the cAMP-producing pathway, adenylate cyclase, ras proteins and the product of CDC25 gene. To determine whether or not the CDC25 gene product is a transducing element in the signal-transmission pathway leading from glucose to ras adenylate cyclase we have made use of the mutated allele RAS2Ile152 whose gene product uncouples the product of CDC25 from adenylate cyclase, but does not promotes other secondary phenotypes. The transient increase in cAMP is lost in cells lacking a functional CDC25 gene product, although they produce a normal amount of cAMP with the RAS2Ile152 gene. This result demonstrates the requirement of CDC25 for mediation of glucose signal transmission. The fact that cells grow normally on glucose in the absence of glucose-induced cAMP signaling confirms that this signaling pathway is not essential for growth on glucose. To further analyze the role of the CDC25 gene product we have made use of truncated versions of the gene. The results show that the C-terminal part of the gene alone is able to mediate glucose-induced activation of the RAS adenylate cyclase pathway.