Hartwell L H
J Cell Biol. 1980 Jun;85(3):811-22. doi: 10.1083/jcb.85.3.811.
Temperature-sensitive mutations that produce insensitivity to division arrest by alpha-factor, a mating pheromone, were isolated in an MATa strain of Saccharomyces cerevisiae and shown by complementation studies to difine eight genes. All of these mutations (designated ste) produce sterility at the restrictive temperature in MATa cells, and mutations in seven of the genes produce sterility in MAT alpha cells. In no case was the sterility associated with these mutations coorectible by including wild-type cells of the same mating type in the mating test nor did nay 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 alpha-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 MATa cells by alpha-factor (agglutinin synthesis as well as division arrest) and for the characteristics that constitutively distinguish MATa from MAT alpha cells (a-factor production, alpha-factor destruction). ste2 Mutants are defective specifically in the two inducible properties, whereas ste4, 5, 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 MAT alpha cells but characteristic of MATa/alpha cells. This study defines seven genes that function in two cell types (MATa and alpha) to control the differentiation of cell type and one gene, ste2, that functions exclusively in MATa cells to mediate responsiveness to polypeptide hormone.
在酿酒酵母的 MATa 菌株中分离出了对 α 因子（一种交配信息素）导致的分裂停滞不敏感的温度敏感突变体，并通过互补研究表明这些突变体定义了八个基因。所有这些突变（命名为 ste）在限制温度下使 MATa 细胞不育，其中七个基因的突变在 MATα 细胞中也导致不育。在任何情况下，这些突变导致的不育都不能通过在交配试验中加入相同交配型的野生型细胞来纠正，并且没有一个突变体抑制野生型细胞的交配；每个基因的突变导致的缺陷似乎是细胞内在的。显然，没有一个突变体仅在对 α 因子的分裂停滞方面有缺陷，因为没有一个突变体的不育被温度敏感的 cdc 28 突变所抑制（后者在正确的细胞周期阶段导致交配时的分裂停滞）。研究了这些突变体对于 α 因子在 MATa 细胞中可诱导的特征（凝集素合成以及分裂停滞）以及对于组成性地区分 MATa 和 MATα 细胞的特征（a 因子产生、α 因子破坏）。ste2 突变体在这两种可诱导特性上有特异性缺陷，而 ste4、5、7、8、9、11 和 12 突变体在组成性以及可诱导方面都有不同程度的缺陷。ste8 和 9 中的突变呈现出一种极性出芽模式，既不像 MATa 细胞也不像 MATα 细胞，但却是 MATa/α 细胞的特征。这项研究定义了七个在两种细胞类型（MATa 和 α）中起作用以控制细胞类型分化的基因，以及一个仅在 MATa 细胞中起作用以介导对多肽激素反应的基因 ste2。
