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J Biol Chem, Vol. 275, Issue 12, 8290-8300, March 24, 2000
From the 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.
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*,
§,, and
Laboratorium voor Moleculaire Celbiologie,
Katholieke Universiteit Leuven, Kardinaal Mercierlaan 92, B-3001
Leuven-Heverlee, Flanders, Belgium and ¶ Department of Cell and
Molecular Biology/Microbiology, Göteborg University, Box 462, S-405 30 Göteborg, Sweden
*
This work was supported by the Commission of the European
Union via Contract FMRX-CT96-0007 (to J. M. T. and S. H.), by a grant from the Swedish Council for Forestry and Agricultural Research SJFR (to S. H.), and by Zuiver Wetenschappelijk Onderzoek "Krediet aan Navorsers" (to M. R.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
The on-line version of this article (available at
http://www.jbc.org) contains supplemental material (Tables S1-S7).
§
Present address: Dept. of Biochemistry, University of Amsterdam,
Academic Medical Centre, Meibergdreef 15, NL-1105 AZ Amsterdam, The Netherlands.
To whom correspondence should be addressed: Dept. of Cell and
Molecular Biology/Microbiology, Göteborg University, Box 462, S-405 30 Göteborg, Sweden. Tel.: 46 31 773 2595; Fax: 46 31 773 2599; E-mail: hohmann@gmm.gu.se.
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