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Title: The transcriptional response of Saccharomyces cerevisiae to osmotic shock - Hot1p and Msn2p/Msn4p are required for the induction of subsets of high osmolarity glycerol pathway-dependent genes
Authors: Rep, M ×
Krantz, M
Thevelein, Johan
Hohmann, S #
Issue Date: 2000
Publisher: AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
Series Title: Journal of Biological Chemistry vol:275 issue:12 pages:8290-8300
Conference: date:Univ Gothenburg, Dept Cell & Mol Biol Microbiol, S-40530 Gothenburg, Sweden; Katholieke Univ Leuven, Lab Mol Celbiol, B-3001 Louvain, Belgium
Abstract: We have analyzed the transcriptional response to osmotic shock in the yeast Saccharomyces cerevisiae. The mRNA level of 186 genes increased at least 3-fold after a shift to NaCl or sorbitol, whereas that of more than 100 genes was at least 1.5-fold diminished. Many induced genes encode proteins that presumably contribute to protection against different types of damage or encode enzymes in glycerol, trehalose, and glycogen metabolism. Several genes, which encode poorly expressed isoforms of enzymes in carbohydrate metabolism, were induced. The high osmolarity glycerol (HOG) pathway is required for full induction of many but not all genes, The recently characterized Hot1p transcription factor is required for normal expression of a subset of the HOG pathway-dependent responses. Stimulated expression of the genes that required the general stress-response transcription factors Msn2p and Msn4p was also reduced in a hog1 mutant, suggesting that Msn2p/Msn4p might be regulated by the HOG pathway. The expression of genes that are known to be controlled by the mating pheromone response pathway was stimulated by osmotic shock specifically in a hog1 mutant. Inappropriate activation of the mating response may contribute to the growth defect of a hog1 mutant in high osmolarity medium.
ISSN: 0021-9258
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Molecular Microbiology and Biotechnology Section - miscellaneous
× corresponding author
# (joint) last author

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