tailieunhanh - Báo cáo khoa học: Transcriptional responses to glucose at different glycolytic rates in Saccharomyces cerevisiae

The addition of glucose toSaccharomyces cerevisiaecells causes reprogramming of gene expression. Glucose is sensed bymembrane receptorsaswell as (so far elusive) intracellular sensing mechanisms. The availability of four yeast strains that display different hexose uptake capacities allowed us to study glucose-induced effects at different glycolytic rates. Rapid glucose responses were observed in all strains able to take up glucose, consistent with intracellular sensing. | Eur. J. Biochem. 271 4855-4864 2004 FEBS 2004 doi Transcriptional responses to glucose at different glycolytic rates in Saccharomyces cerevisiae Karin Elbing1 Anders Stahlberg1 Stefan Hohmann2 and Lena Gustafsson1 1Department of Chemistry and Bioscience-Molecular Biotechnology Chalmers University of Technology Goteborg Sweden department of Cell and Molecular Biology-Microbiology Goteborg University Goteborg Sweden The addition of glucose to Saccharomyces cerevisiae cells causes reprogramming of gene expression. Glucose is sensed by membrane receptors as well as so far elusive intracellular sensing mechanisms. The availability of four yeast strains that display different hexose uptake capacities allowed us to study glucose-induced effects at different glycolytic rates. Rapid glucose responses were observed in all strains able to take up glucose consistent with intracellular sensing. The degree of long-term responses however clearly correlated with the glycolytic rate glucose-stimulated expression of genes encoding enzymes of the lower part of glycolysis showed an almost linear correlation with the glycolytic rate while expression levels of genes encoding gluconeogenic enzymes and invertase SUC2 showed an inverse correlation. Glucose control of SUC2 expression is mediated by the Snf1-Mig1 pathway. Mig1 dephosphorylation upon glucose addition is known to lead to repression of target genes. Mig1 was initially dephosphorylated upon glucose addition in all strains able to take up glucose but remained dephospho rylated only at high glycolytic rates. Remarkably transient Mig1-dephosphorylation was accompanied by the repression of SUC2 expression at high glycolytic rates but stimulated SUC2 expression at low glycolytic rates. This suggests that Mig1-mediated repression can be overruled by factors mediating induction via a low glucose signal. At low and moderate glycolytic rates Mig1 was partly dephosphorylated both in the presence of .