Mutants of Saccharomyces Cerevisiae unresponsive to cell division control by polypeptide mating hormone

Temperature-sensitive mutations that produce insensitivity to division arrest by α-factor, a mating pheromone, were isolated in an MA Ta strain of Saccharomyces cerevisiae and shown by complementation studies to define eight genes. All of these mutations (designated ste) produce sterility at the restrictive temperature in MA Ta cells, and mutations in seven of the genes produce sterility in MATα cells. In no case was the sterility associated with these mutations correctible by including wild-type cells of the same mating type in the mating test nor did any of the mutants inhibit mating of the wild-type cells; the defect appears to be intrinsic to the cell for mutations in each of the genes. Apparently, none of the mutants is defective exclusively in division arrest by α-factor, as the sterility of none is suppressed by a temperature-sensitive cdc 28 mutation (the latter imposes division arrest at the correct cell cycle stage for mating). The mutants were examined for features that are inducible in MA Ta cells by a-factor (agglutinin synthesis as well as division arrest) and for the characteristics that constitutively distinguish MATa from MATα cells (α-factor production, afactor destruction). ste2 Mutants are defective specifically in the two inducible properties, whereas ste4, S, 7, 8, 9, 11, and 12 mutants are defective, to varying degrees, in constitutive as well as inducible aspects. Mutations in ste8 and 9 assume a polar budding pattern unlike either MATa or MATα cells but characteristic of MATa/α cells. This study defines seven genes that function in two cell types (MATa and α) to control the differentiation ofcell type and one gene, stet, that functions exclusively in MA Ta cells to mediate responsiveness to polypeptide hormone.