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A more recent version of this article appeared on September 1, 2002
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Submitted on December 4, 2001
Revised on April 29, 2002
Accepted on June 13, 2002
1 School of Biochemistry and Genetics, University of Newcastle upon Tyne, Newcastle NE2 4HH, UK
2 School of Biochemistry and Genetics, University of Newcastle upon Tyne, Newcastle NE2 4HH, UK (present address: Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK)
3 Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Wilmslow Road, Manchester M20 4BX, UK
4 Biology Department, Boston College, Chestnut Hill, MA 02467, USA
* Corresponding author. E-mail address: S.K.Whitehall{at}ncl.ac.uk.
In Schizosaccharomyces pombe the Sty1 MAP kinase and the Atf1 transcription factor control transcriptional induction in response to elevated salt concentrations. Here we demonstrate that two repressors, Tup11 and Tup12, and the Prr1 transcription factor also function in the response to salt shock. We find that deletion of both tup genes together results in hypersensitivity to elevated cation concentrations (K+ and Ca2+) and we identify cta3+, which encodes an intracellular cation transporter, as a novel stress gene whose expression is positively controlled by the Sty1 pathway and negatively regulated by Tup repressors. The expression of cta3+ is maintained at low levels by the Tup repressors and relief from repression requires the Sty1, Atf1 and Prr1. Prr1 is also required for KCl-mediated induction of several other Sty1-dependent genes such as gpx1+ and ctt1+. Surprisingly, the KCl-mediated induction of cta3+ expression occurs independently of Sty1 in a tup11
tup12 mutant and so the Tup repressors link induction to the Sty1-pathway. We also report that in contrast to a number of other Sty1 and Atf1-dependent genes, the expression of cta3+ is induced only by high salt concentrations. However, in the absence of the Tup repressors this specificity is lost and a range of stresses induce cta3+ expression.
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