title: Regulatory mechanism for expression of GPX1 in response to glucose starvation and Ca in Saccharomyces cerevisiae: involvement of Snf1 and Ras/cAMP pathway in Ca signaling.
abstract: Saccharomyces cerevisiae has three homologues of the glutathione peroxidase gene, GPX1, GPX2, and GPX3. We have previously reported that the expression of GPX3 was constitutive, but that of GPX2 was induced by oxidative stress and CaCl(2), and uncovered the regulatory mechanisms involved. Here, we show that the expression of GPX1 is induced by glucose starvation and treatment with CaCl(2). The induction of GPX1 expression in response to glucose starvation and Ca(2+) was dependent on the transcription factors Msn2 and Msn4 and cis-acting elements [stress response element (STRE)] in the GPX1 promoter. The Ras/cAMP pathway is also involved in the expression of GPX1. We found that Snf1, a Ser/Thr protein kinase, is involved in the glucose starvation- and Ca(2+)-induced expression of GPX1. The activation of Snf1 is accompanied by phosphorylation of Thr(210). We found that the Ca(2+)-treatment as well as glucose starvation causes the phosphorylation of Thr(210) of Snf1 in a Tos3, Sak1, and Elm1 protein kinase-dependent manner. As the timing of the initiation of Ca(2+)-induced expression of GPX1 was retarded in an snf1Delta mutant, the activation of Snf1 seems pivotal to the early-stage-response of GPX1 to Ca(2+).
authors.affiliation: Laboratory of Molecular Microbiology, Division of Applied Life Sciences, Graduate School of Agriculture, Kyoto University, Uji, Kyoto 611-0011, Japan.
authors.forename: Takumi
authors.initials: T
authors.lastname: Ohdate
authors.forename: Shingo
authors.initials: S
authors.lastname: Izawa
authors.forename: Keiko
authors.initials: K
authors.lastname: Kita
authors.forename: Yoshiharu
authors.initials: Y
authors.lastname: Inoue
mesh_terms: D002118:Calcium / Q000494:pharmacology*; D020013:Calcium Signaling / Q000187:drug effects; D000242:Cyclic AMP / Q000378:metabolism; D015966:Gene Expression Regulation, Fungal / Q000187:drug effects*; D005947:Glucose / Q000172:deficiency* / Q000494:pharmacology; D005979:Glutathione Peroxidase / Q000235:genetics* / Q000378:metabolism; D008954:Models, Biological; D009154:Mutation / Q000235:genetics; D009584:Nitrogen / Q000172:deficiency / Q000494:pharmacology; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D020218:Response Elements / Q000235:genetics; D012441:Saccharomyces cerevisiae / Q000166:cytology / Q000201:enzymology* / Q000235:genetics / Q000254:growth & development; D029701:Saccharomyces cerevisiae Proteins / Q000378:metabolism*; D013312:Stress, Physiological / Q000187:drug effects / Q000235:genetics; D018631:ras Proteins / Q000378:metabolism*; D000094765:Glutathione Peroxidase GPX1
chemical_list: D029701:Saccharomyces cerevisiae Proteins; D000242:Cyclic AMP; D005979:Glutathione Peroxidase; C071570:SNF1-related protein kinases; D017346:Protein Serine-Threonine Kinases; C489015:RAS2 protein, S cerevisiae; D018631:ras Proteins; D005947:Glucose; D009584:Nitrogen; D002118:Calcium; D000094765:Glutathione Peroxidase GPX1