| http://purl.uniprot.org/citations/10880465 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/10880465 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/10880465 | http://www.w3.org/2000/01/rdf-schema#comment | "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."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.org/dc/terms/identifier | "doi:10.1093/genetics/155.3.1005"xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.org/dc/terms/identifier | "doi:10.1093/genetics/155.3.1005"xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/author | "Schultz J."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/author | "Schultz J."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/author | "Jigami Y."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/author | "Jigami Y."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/author | "Cullen P.J."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/author | "Cullen P.J."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/author | "Stevenson B.J."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/author | "Stevenson B.J."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/author | "Sprague G.F. Jr."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/author | "Sprague G.F. Jr."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/author | "Horecka J."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/author | "Horecka J."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/date | "2000"xsd:gYear |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/date | "2000"xsd:gYear |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/name | "Genetics"xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/name | "Genetics"xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/pages | "1005-1018"xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/pages | "1005-1018"xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/title | "Defects in protein glycosylation cause SHO1-dependent activation of a STE12 signaling pathway in yeast."xsd:string |
| http://purl.uniprot.org/citations/10880465 | http://purl.uniprot.org/core/title | "Defects in protein glycosylation cause SHO1-dependent activation of a STE12 signaling pathway in yeast."xsd:string |