The DAF2-2 mutation, a dominant inhibitor of the STE4 step in the alpha-factor signaling pathway of Saccharomyces cerevisiae MAT alpha cells.
A dominant mutation (DAF2-2) resulting in resistance to the mating pheromone alpha-factor in Saccharomyces cerevisiae MATa cells was identified and characterized genetically. Whereas wild-type cells induce a high level of the FUS1 mRNA from a low baseline on exposure to alpha-factor, DAF2-2 cells were constitutive producers of an intermediate level of FUS1 RNA; the level was increased only modestly by alpha-factor. FUS1 constitutivity required STE4, STE5 and STE18, but did not require STE2, the alpha-factor receptor gene. DAF2-2 suppressed the alpha-factor supersensitivity of a STE2 C-terminal truncation, and suppressed lethality due to scg1 mutations. Thus DAF2-2 may act by uncoupling the signaling pathway from alpha-factor binding at some point in the pathway between Scg1 inactivation and the action of Ste4, Ste5 and Ste18; this uncoupling might occur at the expense of partial constitutive activation of the pathway. DAF2-2 suppressed the unconditional cell-cycle arrest phenotype of a dominant "constitutive signaling" allele of STE4 (STE4Hpl), although the constitutive FUS1 phenotype of DAF2-2 was suppressed by ste4 null mutations; therefore DAF2-2 may directly affect the performance of the STE4 step.
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Rockefeller University, New York, New York 10021.
D000483:Alleles; D004352:Drug Resistance, Microbial / Q000235:genetics; D004843:Epistasis, Genetic; D015966:Gene Expression Regulation, Fungal; D005800:Genes, Fungal; D000072235:Mating Factor; D009154:Mutation; D010455:Peptides / Q000494:pharmacology*; D010641:Phenotype; D010675:Pheromones / Q000494:pharmacology*; D012441:Saccharomyces cerevisiae / Q000235:genetics*; D015398:Signal Transduction
D010455:Peptides; D010675:Pheromones; D000072235:Mating Factor