Glucose-induced cAMP signaling in Saccharomyces cerevisiae is mediated by the CDC25 protein.
Functional mapping of the cell cycle START gene CDC25 has revealed two domains which are dispensable for viability (germination and growth in glucose media), but are essential for sporulation and differentially involved in glucose-induced cAMP signaling. The transient rise of cAMP is completely prevented by various deletions within the amino-terminal half (alpha domain) of the CDC25 gene product. In contrast, the deletion of the carboxy-terminal 38 residues (beta 2 domain) results in a rapid, but persisting, rise of cAMP. Our data suggest that the alpha domain of the CDC25 protein is involved in glucose signal transduction, whereas the beta 2 domain is required for downregulating the cAMP control chain.
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Max-Planck-Institut für experimentelle Medizin, Abteilung Chemie, Göttingen, FRG.
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D002453:Cell Cycle; D018797:Cell Cycle Proteins; D000242:Cyclic AMP / Q000502:physiology*; D004252:DNA Mutational Analysis; D005656:Fungal Proteins / Q000235:genetics / Q000502:physiology*; D005947:Glucose / Q000502:physiology*; D015183:Restriction Mapping; D012441:Saccharomyces cerevisiae / Q000502:physiology*; D013329:Structure-Activity Relationship; D020666:ras-GRF1
D018797:Cell Cycle Proteins; D005656:Fungal Proteins; D020666:ras-GRF1; D000242:Cyclic AMP; D005947:Glucose