Eight independently isolated mutants which are supersensitive (Sst-) to the Gl arrest induced by the tridecapeptide pheromone a factor were identified by screening mutagenized Saccharomyces cerevisiae MATa cells on solid medium for increased growth inhibition by a factor. These mutants carried lesions in two complementation groups, sstl and sst2. Mutations at the sstl locus were mating type specific: MATa sstl cells were supersensitive to a factor, but MATa sstl cells were not supersensitive to a factor. In contrast, mutations at the sst2 locus conferred supersensitivity to the pheromones of the opposite mating type on both MATa and MATa cells. Even in the absence of added a pheromone, about 10%o of the cells in exponentially growing cultures of MATa strains carrying any of three different alleles of sst2 (including the ochre mutation sst24) had the aberrant morphology ("shmoo" shape) that normally develops only after MATa cells are exposed to a factor. This "self-shmooing" phenotype was genetically linked to the sst2 mutations, although the leakiest allele isolated (sst2-3) did not display this characteristic. Normal MATaIMATa diploids do not respond to pheromones; diploids homozygous for an sst2 mutation (MATa/MATTa sst2-l/sst2-1) were still insensitive to a factor. The sstl gene was mapped to within 6.9 centimorgans of his6 on chromosome IX. The sst2 gene was unlinked to sstl, was not centromere linked, and was shown to be neither linked to nor centromere distal to MAT on the right arm of chromosome III.

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Saccharomyces cerevisiae MATa cells carrying mutations in either sstl or sst2 are supersensitive to the Gl arrest induced by a factor pheromone. When sstl mutants were mixed with normal SSTP cells, the entire population recovered together from a factor arrest, suggesting that SST+ cells helped sstl mutants to recover. Complementation tests and linkage analysis showed that sstl and barl, a mutation which eliminates the ability of MATa cells to act as a "barrier" to the diffusion of a factor, were lesions in the same genes. These findings suggest that sstl mutants are defective in recovery from a factor arrest because they are unable to degrade the pheromone. In contrast, recovery of sst2 mutants was not potentiated by the presence of SSTP cells in mixing experiments. When either normal MATa cells or mutant cells carrying defects in sstl or sst2 were exposed to a factor for 1 h and then washed free of the pheromone, the sst2 cells subsequently remained arrested in the absence of a factor for a much longer time than SSP or sstl cells. These observations suggest that the defect in sst2 mutants is intrinsic to the cell and is involved in the mechanism of a factor action at some step after the initial interaction of the pheromone with the cell. The presence of an sst2 mutation appears to cause a growth debility, since repeated serial subculture of haploid sst2-1 strains led to the accumulation of faster-growing revertants that were pheromone resistant and were mating defective ("sterile").