| Title: | "The DAF2-2 mutation, a dominant inhibitor of the STE4 step in the alpha-factor signaling pathway of Saccharomyces cerevisiae MAT alpha cells" |
| Address: | "Rockefeller University, New York, New York 10021" |
| DOI: | 10.1093/genetics/126.2.301 |
| ISSN/ISBN: | 0016-6731 (Print) 0016-6731 (Linking) |
| Abstract: | "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" |
| Keywords: | "Alleles Drug Resistance, Microbial/genetics Epistasis, Genetic Gene Expression Regulation, Fungal Genes, Fungal Mating Factor *Mutation Peptides/*pharmacology Phenotype Pheromones/*pharmacology Saccharomyces cerevisiae/*genetics *Signal Transduction;" |
| Notes: | "MedlineCross, F R eng GM26176/GM/NIGMS NIH HHS/ Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. 1990/10/01 Genetics. 1990 Oct; 126(2):301-8. doi: 10.1093/genetics/126.2.301" |
