Saccharomyces cerevisiae MATa cells carrying mutations in either sst1 or sst2 are supersensitive to the G1 arrest induced by α factor pheromone. When sst1 mutants were mixed with normal SST⁺ cells, the entire population recovered together from α factor arrest, suggesting that SST⁺ cells helped sst1 mutants to recover. Complementation tests and linkage analysis showed that sst1 and bar1, a mutation which eliminates the ability of MATa cells to act as a “barrier” to the diffusion of α factor, were lesions in the same genes. These findings suggest that sst1 mutants, are defective in recovery from α factor arrest because they are unable to degrade the pheromone. In contrast, recovery of sst2 mutants was not potentiated by the presence of SST⁺ cells in mixing experiments. When either normal MATa cells or mutant cells carrying defects in sst1 or sst2 were exposed to α factor for 1 h and then washed free of the pheromone, the sst2 cells subsequently remained arrested in the absence of α factor for a much longer time than SST⁺ or sst1 cells. These observations suggest that the defect in sst2 mutants is intrinsic to the cell and is involved in the mechanism of α 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”).