SUMMARY: Addition of glucose or related fermentable sugars to derepressed cells of the yeast triggers a RAS-protein-mediated cAMP signal, which induces a protein phosphorylation cascade. Yeast strains without a functional gene were deficient in basal cAMP synthesis and in the glucose-induced cAMP signal. Addition of dinitrophenol, which in wild-type strains strongly stimulates cAMP synthesis by lowering intracellular pH, did not enhance the cAMP level. disruption mutants, in which the basal cAMP level was restored by the oncogene or by disruption of the gene () coding for the high-affinity phosphodiesterase, were still deficient in the glucose- and acidification-induced cAMP responses. These results indicate that the gene product is required not only for basal cAMP synthesis in yeast but also for specific activation of cAMP synthesis by the signal transmission pathway leading from glucose to adenyl cyclase. They also show that intracellular acidification stimulates the pathway at or upstream of the CDC25 protein. When shifted to the restrictive temperature, cells with the temperature sensitive -5 mutation lost their cAMP content within a few minutes. After prolonged incubation at the restrictive temperature, cells with this mutation, and also those with the temperature sensitive mutation, arrested at the ‘start’ point (in G) of the cell cycle, and subsequently accumulated in the resting state G. In contrast with cells, however, the cAMP level did not decrease and normal glucose- and acidification-induced cAMP responses were observed when cells were shifted to the restrictive temperature. These results show that, in the original genetic background at least, growth arrest of -bearing cells at the restrictive temperature is not due to cAMP deficiency. Previous experiments have provided evidence for the presence of a glucose-repressible protein in the signalling pathway. Exponential-phase glucose-grown cells of a strain with overexpression of unexpectedly showed a glucose-induced cAMP signal. Control experiments, however, indicated that overexpression of caused a defect in glucose repression. Introduction of the derepression mutation in the strain with overexpression of restored glucose repression and abolished the glucose-induced cAMP signal, indicating that the CDC25 protein is not the glucose-repressible component of the signalling pathway.


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