The high-affinity glucose uptake system is not required for induction of the RAS-mediated cAMP signal by glucose in cells of the yeast Saccharomyces cerevisiae

Abstract

Addition of glucose or related fermentable sugars to yeast cells grown on non-fermentable carbon sources, triggers a RAS-protein mediated cAMP signal which induces a protein phosphorylation cascade. The high-affinity glucose uptake system in yeast cells is known to be glucose-repressible and only functional in strains containing at least one active kinase. In strains containing point or disruption mutations in the SNF3 gene, which codes for the high-affinity glucose carrier, the glucose-induced cAMP signal is still present. This indicates that the previously demonstrated requirement of a functional kinase for the induction of the cAMP signal, does not reflect requirement of high-affinity sugar transport. It also indicates that the unknown glucose-repressible protein in the induction sequence of the RAS-mediated cAMP signal is not the high-affinity sugar carrier.