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dc.contributor.authorGreenall, Amanda
dc.contributor.authorHadcroft, Andrew P
dc.contributor.authorMalakasi, Panagiota
dc.contributor.authorJones, Nic
dc.contributor.authorMorgan, Brian A
dc.contributor.authorHoffman, Charles S
dc.contributor.authorWhitehall, Simon K
dc.date.accessioned2009-10-05T15:59:15Z
dc.date.available2009-10-05T15:59:15Z
dc.date.issued2002-09
dc.identifier.citationRole of fission yeast Tup1-like repressors and Prr1 transcription factor in response to salt stress. 2002, 13 (9):2977-89 Mol. Biol. Cellen
dc.identifier.issn1059-1524
dc.identifier.pmid12221110
dc.identifier.doi10.1091/mbc.01-12-0568
dc.identifier.urihttp://hdl.handle.net/10541/83581
dc.description.abstractIn Schizosaccharomyces pombe, the Sty1 mitogen-activated protein kinase and the Atf1 transcription factor control transcriptional induction in response to elevated salt concentrations. Herein, 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 Ca(2+)) 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 tup11Delta tup12Delta 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 induces cta3(+) expression.
dc.language.isoenen
dc.subject.meshBiological Transport
dc.subject.meshCations
dc.subject.meshDose-Response Relationship, Drug
dc.subject.meshGene Expression Regulation, Fungal
dc.subject.meshIons
dc.subject.meshModels, Biological
dc.subject.meshNuclear Proteins
dc.subject.meshPhenotype
dc.subject.meshPlasmids
dc.subject.meshPotassium
dc.subject.meshPrecipitin Tests
dc.subject.meshPromoter Regions, Genetic
dc.subject.meshProtein Binding
dc.subject.meshRNA
dc.subject.meshRepressor Proteins
dc.subject.meshSaccharomyces cerevisiae Proteins
dc.subject.meshSalts
dc.subject.meshSchizosaccharomyces
dc.subject.meshSchizosaccharomyces pombe Proteins
dc.subject.meshTime Factors
dc.subject.meshTranscription Factors
dc.subject.meshbeta-Galactosidase
dc.titleRole of fission yeast Tup1-like repressors and Prr1 transcription factor in response to salt stress.en
dc.typeArticleen
dc.contributor.departmentSchool of Biochemistry and Genetics, University of Newcastle upon Tyne, United Kingdom.en
dc.identifier.journalMolecular Biology of the Cellen
html.description.abstractIn Schizosaccharomyces pombe, the Sty1 mitogen-activated protein kinase and the Atf1 transcription factor control transcriptional induction in response to elevated salt concentrations. Herein, 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 Ca(2+)) 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 tup11Delta tup12Delta 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 induces cta3(+) expression.


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