title: Role of STE genes in the mating factor signaling pathway mediated by GPA1 in Saccharomyces cerevisiae.
abstract: The ste mutants (ste2, ste4, ste5, ste7, ste11, and ste12) are insensitive to mating factors and are, therefore, sterile. Roles of the STE gene products in the GPA1-mediated mating factor signaling pathway were studied by using ste gpa1 double mutants. Mating efficiency of a ste2 mutant defective in the alpha-factor receptor increased 1,000-fold in a gpa1 background, while G1 arrest and aberrant morphology (shmoo) caused by gpa1 were not suppressed by ste2. Furthermore, the steady-state level of the FUS1 transcript, which normally increases in response to mating factors, was also elevated when the GPA1 function was impaired. These results suggest that the GPA1 protein functions downstream of the STE2 receptor. Conversely, the sterility of ste4, ste5, ste7, ste11, and ste12 mutants was not suppressed by gpa1, but the lethal phenotype of gpa1 was suppressed by these ste mutations. Northern (RNA) blotting analysis revealed that the ste7, ste11, and ste12 mutations caused reductions of 50 to 70% in the steady-state levels of the GPA1 transcript, while ste4 had a slight effect and ste5 had no effect. This implies that the suppression by ste7, ste11, and ste12 could be due to reduced syntheses of additional components, including an effector, and that suppression by ste4 and ste5 may result from direct effects on the signaling pathway. The STE4, STE5, STE7, STE11, and STE12 products, therefore, appear to specify components of the signal transduction machinery, directly or indirectly, which function together with or downstream of GPA1.
authors.affiliation: Department of Molecular Biology, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, California 94304.
authors.forename: N
authors.initials: N
authors.lastname: Nakayama
authors.forename: Y
authors.initials: Y
authors.lastname: Kaziro
authors.forename: K
authors.initials: K
authors.lastname: Arai
authors.forename: K
authors.initials: K
authors.lastname: Matsumoto
mesh_terms: D003433:Crosses, Genetic; D005800:Genes, Fungal; D005838:Genotype; D000072235:Mating Factor; D009154:Mutation; D010455:Peptides / Q000502:physiology*; D010957:Plasmids; D012441:Saccharomyces cerevisiae / Q000235:genetics* / Q000254:growth & development / Q000502:physiology; D015398:Signal Transduction
chemical_list: D010455:Peptides; D000072235:Mating Factor