These two authors contributed equally to this paper.
Molecular cloning of a gene involved in glucose sensing in the yeast Saccharomyces cerevisiae
Article first published online: 27 OCT 2006
Volume 8, Issue 5, pages 927–943, May 1993
How to Cite
Van Aelst, L., Hohmann, S., Bulaya, B., de Koning, W., Sierkstra, L., Neves, M. J., Luyten, K., Alijo, R., Ramos, J., Coccetti, P., Martegani, E., de Magalhães-Rocha, N. M., Brandão, R. L., Van Dijck, P., Vanhalewyn, M., Durnez, P., Arnold W. H. Jans and Thevelein, J. M. (1993), Molecular cloning of a gene involved in glucose sensing in the yeast Saccharomyces cerevisiae. Molecular Microbiology, 8: 927–943. doi: 10.1111/j.1365-2958.1993.tb01638.x
- Issue published online: 27 OCT 2006
- Article first published online: 27 OCT 2006
- Received 25 November, 1992; revised and accepted 15 February, 1993.
Cells of the yeast Saccharomyces cerevisiae display a wide range of glucose-induced regulatory phenomena, including glucose-induced activation of the RAS-adenylate cyclase pathway and phosphatidylinositol turnover, rapid post-translational effects on the activity of different enzymes as well as long-term effects at the transcriptional level. A gene called GGS1 (for General Glucose Sensor) that is apparently required for the glucose-induced regulatory effects and several ggs1 alleles (fdp1, byp1 and cif1) has been cloned and characterized. A GGS1 homologue is present in Methanobacterium thermoautotrophicum. Yeast ggs1 mutants are unable to grow on glucose or related readily fermentable sugars, apparently owing to unrestricted influx of sugar into glycolysis, resulting in its rapid deregulation. Levels of intracellular free glucose and metabolites measured over a period of a few minutes after addition of glucose to cells of a ggsi1Δ strain are consistent with our previous suggestion of a functional interaction between a sugar transporter, a sugar kinase and the GGS1 gene product. Such a glucose-sensing system might both restrict the influx of glucose and activate several signal transduction pathways, leading to the wide range of glucose-induced regulatory phenomena. Deregulation of these pathways in ggs1 mutants might explain phenotypic defects observed in the absence of glucose, e.g. the inability of ggs1 diploids to sporulate.