Regulatory mechanism for expression of GPX1 in response to glucose starvation and Ca²⁺ in Saccharomyces cerevisiae: involvement of Snf1 and Ras/cAMP pathway in Ca²⁺ signaling

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 CaCl₂, and uncovered the regulatory mechanisms involved. Here, we show that the expression of GPX1 is induced by glucose starvation and treatment with CaCl₂. The induction of GPX1 expression in response to glucose starvation and Ca²⁺ 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 Ca²⁺-induced expression of GPX1. The activation of Snf1 is accompanied by phosphorylation of Thr²¹⁰. We found that the Ca²⁺-treatment as well as glucose starvation causes the phosphorylation of Thr²¹⁰ of Snf1 in a Tos3, Sak1, and Elm1 protein kinase-dependent manner. As the timing of the initiation of Ca²⁺-induced expression of GPX1 was retarded in an snf1Δ mutant, the activation of Snf1 seems pivotal to the early-stage-response of GPX1 to Ca²⁺.