Activation of the Saccharomyces cerevisiae filamentation/invasion pathway by osmotic stress in high-osmolarity glycogen pathway mutants

• Published in: Genetics (Austin) Vol. 153; no. 3; pp. 1091 - 1103
• Main Authors: Davenport, K.D, Williams, K.E, Ullmann, B.D, Guston, M.C
• Format: Journal Article
• Language: English
• Published: Legacy CDMS Genetics Soc America 01.11.1999
• Subjects: alleles; Cloning, Molecular; deletions; gene expression; genes; Genotype; glycerol; Glycerol - metabolism; Glycogen - genetics; gpd1 gene; hyperosmotic shock; hypertonic stress; kss1 gene; Life Sciences (General); messenger RNA; mitogen-activated protein kinase; Mitogen-Activated Protein Kinase Kinases - genetics; Mitogen-Activated Protein Kinase Kinases - metabolism; Mitogen-Activated Protein Kinases - metabolism; mutants; Osmolar Concentration; osmotic pressure; phosphoprotein phosphatase; phosphorylation; proteins; Saccharomyces cerevisiae; Saccharomyces cerevisiae - genetics; Saccharomyces cerevisiae - growth & development; Saccharomyces cerevisiae - physiology; Saccharomyces cerevisiae Proteins; Signal Transduction; Sorbitol - pharmacology; stress; Suppression, Genetic - drug effects; suppressors; tec1 gene; transcription (genetics); Transcription, Genetic; Non-Nasa Center; Nasa Discipline Cell Biology; NASA Discipline Cell Biology; Non-NASA Center
• ISSN: 0016-6731; 1943-2631; 1943-2631
• DOI: 10.1093/genetics/153.3.1091

Mitogen-activated protein kinase (MAPK) cascades are frequently used signal transduction mechanisms in eukaryotes. Of the five MAPK cascades in Saccharomyces cerevisiae, the high-osmolarity glycerol response (HOG) pathway functions to sense and respond to hypertonic stress. We utilized a partial loss-of-function mutant in the HOG pathway, pbs2-3, in a high-copy suppressor screen to identify proteins that modulate growth on high-osmolarity media. Three high-copy suppressors of pbs2-3 osmosensitivity were identified: MSG5, CAK1, and TRX1. Msg5p is a dual-specificity phosphatase that was previously demonstrated to dephosphorylate MAPKs in yeast. Deletions of the putative MAPK targets of Msg5p revealed that kss1delta could suppress the osmosensitivity of pbs2-3. Kss1p is phosphorylated in response to hyperosmotic shock in a pbs2-3 strain, but not in a wild-type strain nor in a pbs2-3 strain overexpressing MSG5. Both TEC1 and FRE::lacZ expressions are activated in strains lacking a functional HOG pathway during osmotic stress in a filamentation/invasion-pathway-dependent manner. Additionally, the cellular projections formed by a pbs2-3 mutant on high osmolarity are absent in strains lacking KSS1 or STE7. These data suggest that the loss of filamentation/invasion pathway repression contributes to the HOG mutant phenotype.