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Molecular and Cellular Biology, August 1999, p. 5474-5485, Vol. 19, No. 8
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Osmotic Stress-Induced Gene Expression in Saccharomyces
cerevisiae Requires Msn1p and the Novel Nuclear Factor
Hot1p
Martijn
Rep,1
Vladimír
Reiser,2
Ulrike
Gartner,2
Johan M.
Thevelein,1
Stefan
Hohmann,1,3,*
Gustav
Ammerer,2 and
Helmut
Ruis2
Laboratorium voor Moleculaire Celbiologie,
Katholieke Universiteit Leuven, B-3001 Heverlee, Flanders,
Belgium1; Institute of Biochemistry and
Molecular Cell Biology and Ludwig Boltzmann-Forschungsstelle für
Biochemie, University of Vienna, A-1030 Vienna,
Austria2; and Department of Cell and
Molecular Biology/Microbiology, Lundberg Laboratory, Göteborg
University, S-405 30 Göteborg, Sweden3
Received 3 March 1999/Returned for modification 8 April
1999/Accepted 28 April 1999
After a sudden shift to high osmolarity, Saccharomyces
cerevisiae cells respond by transiently inducing the expression
of stress-protective genes. Msn2p and Msn4p have been described as two
transcription factors that determine the extent of this response. In
msn2 msn4 mutants, however, many promoters still show a
distinct rise in transcriptional activity upon osmotic stress. Here we describe two structurally related nuclear factors, Msn1p and a newly
identified protein, Hot1p (for high-osmolarity-induced transcription), which are also involved in osmotic stress-induced transcription. hot1 single mutants are specifically compromised in the
transient induction of GPD1 and GPP2, which
encode enzymes involved in glycerol biosynthesis, and exhibit delayed
glycerol accumulation after stress exposure. Similar to a
gpd1 mutation, a hot1 defect can rescue cells
from inappropriately high HOG pathway activity. In contrast, Hot1p has
little influence on the osmotic stress induction of CTT1,
where Msn1p appears to play a more prominent role. Cells lacking Msn1p,
Msn2p, Msn4p, and Hot1p are almost devoid of the short-term
transcriptional response of the genes GPD1,
GPP2, CTT1, and HSP12 to osmotic
stress. Such cells also show a distinct reduction in the nuclear
residence of the mitogen-activated protein kinase Hog1p upon osmotic
stress. Thus, Hot1p and Msn1p may define an additional tier of
transcriptional regulators that control responses to high-osmolarity stress.
*
Corresponding author. Mailing address: Department of
Cell and Molecular Biology/Microbiology, Göteborg University, Box
462, S-405 30 Göteborg, Sweden. Phone: 46-31-7732595. Fax:
46-31-7732599. E-mail: hohmann{at}gmm.gu.se.
Molecular and Cellular Biology, August 1999, p. 5474-5485, Vol. 19, No. 8
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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