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Title: Molecular cloning of a gene involved in glucose sensing in the yeast Saccharomyces cerevisiae.
Authors: Aelst, Linda Van
Hohmann, Stefan
Bulaya, Botchaka
Koning, Wim de
Sierkstra, Laurens
Neves, Maria José
Luyten, Kattie
Alijo, Rafael
Ramos, José
Coccetti, Paola
Martegani, Enzo
Rocha, Neuza Maria de Magalhaes
Brandão, Rogélio Lopes
Dijck, Patrick Van
Vanhalewyn, Mieke
Durnez, Peter
Jans, Arnold W. H
Thevelein, Johan Maria
Issue Date: 1993
Citation: AELST, L. V et al. Molecular cloning of a gene involved in glucose sensing in the yeast Saccharomyces cerevisiae. Molecular Microbiology, v. 82, p. 927-943, 1993. Disponível em: <>. Acesso em: 10 jan. 2017.
Abstract: 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 phosphatidylinosrtot turnover, rapid post-translatronal 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 ggsi aHeles (fic/pf, bypi and cifi) has been cloned and characterized. A GGS1 homologue is present in Methanobacterium thermoautotrophicum. Yeast ggsi mutants are unable to grow on glucose or Received 25 November, 1992; revised and accepted 15 February, 1993. •For correspondence. Tel. (16) 220931; Fax (16) 204415. tThese two authors contributed equally to this paper. 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 ggsi^ 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 ggsi mutants might explain phenotypic defects observed in the absence of glucose, e.g. the inability of ggsi diploids to sporulate.
ISSN: 1365-2958
Appears in Collections:DEFAR - Artigos publicados em periódicos

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