The Ssn6-Tup1 repressor complex of Saccharomyces cerevisiae is involved in the osmotic induction of HOG-dependent and -independent genes

Märquez, JoséA

doi:10.1093/emboj/17.9.2543

Cited by 67 publications

(67 citation statements)

References 62 publications

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“…The regulation of HAL1 gene expression has been previously reported to depend on a repression mechanism occurring on an upstream promoter region, URS HAL1 (Ϫ231 to Ϫ156) (23). A database search (MatInspector 34) revealed a CRE-like sequence at position Ϫ222 to Ϫ215.…”

Section: Resultsmentioning

confidence: 99%

“…The GST-Sko1 fusion protein was tested for CRE HAL1 interaction as described previously (33). Binding conditions for His-tagged Gcn4 protein and general conditions of electrophoresis were as described previously (23). Yeast protein extracts were prepared as in reference (23).…”

Section: Methodsmentioning

confidence: 99%

“…Binding conditions for His-tagged Gcn4 protein and general conditions of electrophoresis were as described previously (23). Yeast protein extracts were prepared as in reference (23). Oligonucleotides representing CRE HAL1 and the point-mutated CRE* HAL1 (the same as that used to construct the corresponding CRE HAL1 -lacZ plasmids) were labeled by filling the SalI protruding ends with Klenow polymerase.…”

Section: Methodsmentioning

confidence: 99%

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The Sko1p Repressor and Gcn4p Activator Antagonistically Modulate Stress-Regulated Transcription in Saccharomyces cerevisiae

Pascual-Ahuir

Serrano

Proft

2001

Molecular and Cellular Biology

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In the transcriptional response of Saccharomyces cerevisiae to stress, both activators and repressors are implicated. Here we demonstrate that the ion homeostasis determinant, HAL1, is regulated by two antagonistically operating bZIP transcription factors, the Sko1p repressor and the Gcn4p activator. A single CRE-like sequence (CRE HAL1 ) at position ؊222 to ؊215 with the palindromic core sequence TTACGTAA is essential for stress-induced expression of HAL1. Down-regulation of HAL1 under normal growth conditions requires specific binding of Sko1p to CRE HAL1 and the corepressor gene SSN6. Release from this repression depends on the function of the high-osmolarity glycerol pathway. The Gcn4p transcriptional activator binds in vitro to the same CRE HAL1 and is necessary for up-regulated HAL1 expression in vivo, indicating a dual control mechanism by a repressor-activator pair occupying the same promoter target sequence. gcn4 mutants display a strong sensitivity to elevated K ؉ or Na ؉ concentrations in the growth medium. In addition to reduced HAL1 expression, this sensitivity is explained by the fact that amino acid uptake is drastically impaired by high Na

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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The Sko1p Repressor and Gcn4p Activator Antagonistically Modulate Stress-Regulated Transcription in Saccharomyces cerevisiae

Pascual-Ahuir

Serrano

Proft

2001

Molecular and Cellular Biology

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“…Network analysis of these regulators showed that many regulators are highly connected and interact with each other genetically and biochemically ( Fig. 8) (5,18,44,59,72,80,81,88,91,95,98,106,120,123,128). Many of the regulators are components of global regulatory complexes.…”

Section: Suppression Of Hypoxia Responsiveness Of a Network Of Regulamentioning

confidence: 99%

Deletion of a subgroup of ribosome-related genes minimizes hypoxia-induced changes and confers hypoxia tolerance

Shah

Cadinu

Henke

et al. 2011

Physiological Genomics

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Deletion of a subgroup of ribosome-related genes minimizes hypoxia-induced changes and confers hypoxia tolerance. Physiol Genomics 43: 855-872, 2011. First published May 17, 2011 doi:10.1152/physiolgenomics.00232.2010.-Hypoxia is a widely occurring condition experienced by diverse organisms under numerous physiological and disease conditions. To probe the molecular mechanisms underlying hypoxia responses and tolerance, we performed a genome-wide screen to identify mutants with enhanced hypoxia tolerance in the model eukaryote, the yeast Saccharomyces cerevisiae.Yeast provides an excellent model for genomic and proteomic studies of hypoxia. We identified five genes whose deletion significantly enhanced hypoxia tolerance. They are RAI1, NSR1, BUD21, RPL20A, and RSM22, all of which encode functions involved in ribosome biogenesis. Further analysis of the deletion mutants showed that they minimized hypoxia-induced changes in polyribosome profiles and protein synthesis. Strikingly, proteomic analysis by using the iTRAQ profiling technology showed that a substantially fewer number of proteins were changed in response to hypoxia in the deletion mutants, compared with the parent strain. Computational analysis of the iTRAQ data indicated that the activities of a group of regulators were regulated by hypoxia in the wild-type parent cells, but such regulation appeared to be diminished in the deletion strains. These results show that the deletion of one of the genes involved in ribosome biogenesis leads to the reversal of hypoxia-induced changes in gene expression and related regulators. They suggest that modifying ribosomal function is an effective mechanism to minimize hypoxia-induced specific protein changes and to confer hypoxia tolerance. These results may have broad implications in understanding hypoxia responses and tolerance in diverse eukaryotes ranging from yeast to humans.genome-wide screen; proteomic analysis; iTRAQ; regulatory network; stress response LIVING ORGANISMS RANGING FROM aquatic organisms to plants and humans can experience episodes of low oxygen availability, namely, hypoxia. Hypoxia can occur in plant roots when a field is flooded, in yeast during fermentation, or in humans at high altitudes or as a result of a heart attack or stroke. Because oxygen is critical for the survival and development of many living organisms, particularly eukaryotes, living organisms ranging from yeast to humans have developed sophisticated mechanisms to respond and adapt to the changes in oxygen levels in the environment (12, 127). In the wilderness, several species, including fossorial mammals, diving animals, and birds living at high altitudes, have acquired hypoxia tolerance, which enables them to survive under conditions of limited oxygen supply (9, 84, 92). In humans, hypoxia is associated with an array of pathological conditions, such as cancer and stroke. Mechanisms of oxygen sensing and regulation have been implicated in a wide array of physiological and pathological processes (35,99,127). Thus, studying hypoxia ...

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“…Total RNA was isolated according to Carlson and Botstein (1982) and Northern blot analysis was performed as described by Má rquez et al (1998). The probes used were PCR fragments spanning the whole CTT1 and HAL2 ORFs or part of the NST1 ORF.…”

Section: Northern Blot Analysismentioning

confidence: 99%

Involvement of Nst1p/YNL091w and Msl1p, a U2B″ splicing factor, in Saccharomyces cerevisiae salt tolerance

Goossens¹,

Forment²,

Serrano³

2002

Yeast

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Cell tolerance to salt stress depends on many physiological functions, including the best characterized of osmotic adjustment, ion transport and sodium-sensitive sulphate metabolism. From a screening designed to identify novel determinants of salt tolerance we have isolated the YNL091w gene, probably an Ascomycete-specific gene encoding a protein of unknown function. This gene negatively affects salt tolerance and therefore has been designated NST1. The salt tolerance mechanism of nst1 mutants is novel because it is not related to osmoregulation, altered cation accumulation or sulphate metabolism. Genome-wide two-hybrid analysis has suggested that Nst1p interacts with the splicing factor Msl1p and, accordingly, the impact of NST1 on salt tolerance is dependent on a functional MSL1 gene. Loss of MSL1 and NST1 function has pleiotropic phenotypes including increased sensitivity to divalent cations (manganese and zinc) and to caffeine (a cell wall-weakening agent). On the other hand, msl1 mutants but not nst1 mutants are sensitive to thiabendazole (a microtubule-destabilizing agent) and to osmotic stress.

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The Ssn6-Tup1 repressor complex of Saccharomyces cerevisiae is involved in the osmotic induction of HOG-dependent and -independent genes

Cited by 67 publications

References 62 publications

The Sko1p Repressor and Gcn4p Activator Antagonistically Modulate Stress-Regulated Transcription in Saccharomyces cerevisiae

The Sko1p Repressor and Gcn4p Activator Antagonistically Modulate Stress-Regulated Transcription in Saccharomyces cerevisiae

Deletion of a subgroup of ribosome-related genes minimizes hypoxia-induced changes and confers hypoxia tolerance

Involvement of Nst1p/YNL091w and Msl1p, a U2B″ splicing factor, in Saccharomyces cerevisiae salt tolerance

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