title: Defects in protein glycosylation cause SHO1-dependent activation of a STE12 signaling pathway in yeast.
abstract: In haploid Saccharomyces cerevisiae, mating occurs by activation of the pheromone response pathway. A genetic selection for mutants that activate this pathway uncovered a class of mutants defective in cell wall integrity. Partial loss-of-function alleles of PGI1, PMI40, PSA1, DPM1, ALG1, MNN10, SPT14, and OCH1, genes required for mannose utilization and protein glycosylation, activated a pheromone-response-pathway-dependent reporter (FUS1) in cells lacking a basal signal (ste4). Pathway activation was suppressed by the addition of mannose to hexose isomerase mutants pgi1-101 and pmi40-101, which bypassed the requirement for mannose biosynthesis in these mutants. Pathway activation was also suppressed in dpm1-101 mutants by plasmids that contained RER2 or PSA1, which produce the substrates for Dpm1. Activation of FUS1 transcription in the mannose utilization/protein glycosylation mutants required some but not all proteins from three different signaling pathways: the pheromone response, invasive growth, and HOG pathways. We specifically suggest that a Sho1 --> Ste20/Ste50 --> Ste11 --> Ste7 --> Kss1 --> Ste12 pathway is responsible for activation of FUS1 transcription in these mutants. Because loss of pheromone response pathway components leads to a synthetic growth defect in mannose utilization/protein glycosylation mutants, we suggest that the Sho1 --> Ste12 pathway contributes to maintenance of cell wall integrity in vegetative cells.
authors.affiliation: Institute of Molecular Biology, University of Oregon, Eugene, Oregon 97403-1229, USA. gsprague@molbio.uoregon.edu
authors.forename: P J
authors.initials: PJ
authors.lastname: Cullen
authors.forename: J
authors.initials: J
authors.lastname: Schultz
authors.forename: J
authors.initials: J
authors.lastname: Horecka
authors.forename: B J
authors.initials: BJ
authors.lastname: Stevenson
authors.forename: Y
authors.initials: Y
authors.lastname: Jigami
authors.forename: G F
authors.initials: GF
authors.lastname: Sprague
mesh_terms: D002473:Cell Wall / Q000235:genetics / Q000378:metabolism; D005656:Fungal Proteins / Q000235:genetics / Q000378:metabolism*; D005816:Genetic Complementation Test; D006031:Glycosylation; D008358:Mannose / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000172:deficiency / Q000235:genetics; D008565:Membrane Proteins / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009154:Mutation; D010675:Pheromones / Q000378:metabolism; D011401:Promoter Regions, Genetic; D011493:Protein Kinase C / Q000378:metabolism; D011993:Recombinant Fusion Proteins / Q000235:genetics / Q000378:metabolism; D012441:Saccharomyces cerevisiae / Q000201:enzymology* / Q000235:genetics / Q000254:growth & development; D029701:Saccharomyces cerevisiae Proteins; D015398:Signal Transduction / Q000235:genetics*; D014157:Transcription Factors / Q000378:metabolism*; D014158:Transcription, Genetic
chemical_list: C490024:FUS1 protein, S cerevisiae; D005656:Fungal Proteins; C066709:GAS1 protein, S cerevisiae; D008562:Membrane Glycoproteins; D008565:Membrane Proteins; D010675:Pheromones; D011993:Recombinant Fusion Proteins; C489241:STE12 protein, S cerevisiae; D029701:Saccharomyces cerevisiae Proteins; D014157:Transcription Factors; D011493:Protein Kinase C; C088589:HOG1 protein, S cerevisiae; D020928:Mitogen-Activated Protein Kinases; D008358:Mannose