Neiman A M, Chang F, Komachi K, Herskowitz I
Department of Biochemistry and Biophysics, University of California, San Francisco 94143.
Cell Regul. 1990 Apr;1(5):391-401. doi: 10.1091/mbc.1.5.391.
Mutations in either the CDC36 or CDC39 gene cause yeast cells to arrest in G1 of the cell cycle at the same point as treatment with mating pheromone. We demonstrate here that strains harboring temperature-sensitive mutations in CDC36 or CDC39 activate expression of the pheromone-inducible gene FUS1 when shifted to nonpermissive temperature. We show further that cell-cycle arrest and induction of FUS1 are dependent on known components of the mating factor response pathway, the STE genes. Thus, the G1-arrest phenotype of cdc36 and cdc39 mutants results from activation of the mating factor response pathway. The CDC36 and CDC39 gene products behave formally as negative elements in the response pathway: they are required to block response in the absence of pheromone. Epistasis analysis of mutants defective in CDC36 or CDC39 and different STE genes demonstrates that activation requires the response pathway G protein and suggests that CDC36 and CDC39 products may control synthesis or function of the G alpha subunit.
CDC36 基因或 CDC39 基因发生突变会导致酵母细胞在细胞周期的 G1 期停滞，停滞点与用交配信息素处理时相同。我们在此证明，携带 CDC36 或 CDC39 温度敏感突变的菌株在转移到非允许温度时会激活信息素诱导基因 FUS1 的表达。我们进一步表明，细胞周期停滞和 FUS1 的诱导依赖于交配因子反应途径的已知组分，即 STE 基因。因此，cdc36 和 cdc39 突变体的 G1 期停滞表型是由交配因子反应途径的激活导致的。CDC36 和 CDC39 基因产物在反应途径中正式表现为负调控元件：在没有信息素的情况下，它们是阻止反应所必需的。对 CDC36 或 CDC39 以及不同 STE 基因缺陷的突变体进行的上位性分析表明，激活需要反应途径 G 蛋白，并提示 CDC36 和 CDC39 产物可能控制 Gα亚基的合成或功能。
