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The HOG MAP kinase pathway is required for the induction of methylglyoxal‐responsive genes and determines methylglyoxal resistance in Saccharomyces cerevisiae
Author(s) -
Aguilera Jaime,
RodríguezVargas Sonia,
Prieto Jose A.
Publication year - 2005
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2005.04533.x
Subject(s) - methylglyoxal , biology , saccharomyces cerevisiae , kinase , microbiology and biotechnology , phosphorylation , biochemistry , signal transduction , gene expression , phosphatase , mutant , mapk/erk pathway , gene , enzyme
Summary A sudden overaccumulation of methylglyoxal (MG) induces, in Saccharomyces cerevisiae , the expression of MG‐protective genes, including GPD1 , GLO1 and GRE 3. The response is partially dependent on the transcriptional factors Msn2p/Msn4p, but unrelated with the general stress response mechanism. Here, we show that the high‐osmolarity glycerol (HOG)‐pathway controls the genetic response to MG and determines the yeast growth capacity upon MG exposure. Strains lacking the MAPK Hog1p, the upstream component Ssk1p or the HOG‐dependent nuclear factor Msn1p, showed a reduction in the mRNA accumulation of MG‐responsive genes after MG addition. Moreover, hyperactivation of Hog1p by deletion of protein phosphatase PTP2 enhanced the response, while blocking the pathway by deletion of the MAPKK PBS 2 had a negative effect. In addition, the activity of Hog1p affected the basal level of GPD1 mRNA under non‐inducing conditions. These effects had a great influence on MG resistance, as hog1 Δ and other HOG‐pathway mutants with impaired MG‐specific expression displayed MG sensitivity, whereas those with enhanced expression exhibited MG resistance as compared with the wild‐type. However, MG does not trigger the overphosphorylation of Hog1p or its nuclear import in the parental strain. Moreover, dual phosphorylation of Hog1p appears to be dispensable in the triggering of the transcriptional response, although a phosphorylable form of Hog1p is fundamental for the transcriptional activity. Overall, our results suggest that the basal activity of the HOG‐pathway serves to amplify the expression of MG‐responsive genes under non‐inducing and inducing conditions, ensuring cell protection against this toxic glycolytic by‐product.