Defects in protein glycosylation cause SHO1-dependent activation of a STE12 signaling pathway in yeast

In haploid Saccharomyces cerevisiae, mating occurs by activation of the phe romone response pathway. A genetic selection for mutants that activate this pathway uncovered a class of mutants defective in cell wall integrity. Par tial loss-of-function alleles of PGI1, PMI40, PSA1, DPM1, ALG1, MNN10, SPT1 4, and OCH1, genes required for mannose utilization and protein glycosylati on, activated a pheromone-response-pathway-dependent reporter (FUS1) in cel ls lacking a basal signal (ste4). Pathway activation was suppressed by the addition of mannose to hexose isomerase mutants pgi1-101 and pmi40-101, whi ch bypassed the requirement for mannose biosynthesis in these mutants. Path way activation was also suppressed in dpm1-101 mutants by plasmids that con tained RER2 or PSA1, which produce the substrates for Dpm1. Activation of F US1 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 mutant s. Because loss of pheromone response pathway components leads to a synthet ic growth defect in mannose utilization/protein glycosylation mutants, we s uggest that the Sho1 --> Ste12 pathway contributes to maintenance of cell w all integrity in vegetative cells.