Irie K, Yamaguchi K, Kawase K, Matsumoto K
Department of Molecular Biology, Faculty of Science, Nagoya University, Japan.
Mol Cell Biol. 1994 May;14(5):3150-7. doi: 10.1128/mcb.14.5.3150-3157.1994.
The STE4 gene encodes the beta subunit of a heterotrimeric G protein that is an essential component of the pheromone signal transduction pathway. To identify downstream component(s) of Ste4, we sought pseudo-revertants that restored mating competence to ste4 mutants. The suppressor mot2 was isolated as a recessive mutation that restored conjugational competence to a temperature-sensitive ste4 mutant and simultaneously conferred a temperature-sensitive growth phenotype. The MOT2 gene encodes a putative zinc finger protein, the deletion of which resulted in temperature-sensitive growth, increased expression of FUS1 in the absence of pheromones, and suppression of a deletion of the alpha-factor receptor. On the other hand, sterility resulting from deletion of STE4 was not suppressed by the mot2 deletion. These phenotypes are similar to those associated with temperature-sensitive mutations in CDC36 and CDC39, which are proposed to encode general negative regulators of transcription rather than factors involved in the pheromone response pathway. Deletion of MOT2 also caused increased transcription of unrelated genes such as GAL7 and PHO84. Overexpression of MOT2 suppresses the growth defect of temperature-sensitive mutations in CDC36 and CDC39. These observations suggest that Mot2 functions as a general negative regulator of transcription in the same processes as Cdc36 and Cdc39.
STE4基因编码异源三聚体G蛋白的β亚基，该蛋白是信息素信号转导途径的重要组成部分。为了鉴定Ste4的下游组分，我们寻找能使ste4突变体恢复交配能力的假回复突变体。抑制子mot2作为隐性突变被分离出来，它能使温度敏感型ste4突变体恢复接合能力，并同时赋予温度敏感型生长表型。MOT2基因编码一种假定的锌指蛋白，其缺失导致温度敏感型生长、在无信息素时FUS1表达增加以及α因子受体缺失的抑制。另一方面，mot2缺失并不能抑制STE4缺失导致的不育。这些表型与CDC36和CDC39中温度敏感型突变相关的表型相似，据推测CDC36和CDC39编码转录的一般负调控因子，而非参与信息素应答途径的因子。MOT2缺失也导致无关基因如GAL7和PHO84的转录增加。MOT2的过表达抑制了CDC36和CDC39中温度敏感型突变的生长缺陷。这些观察结果表明，Mot2在与Cdc36和Cdc39相同的过程中作为转录的一般负调控因子发挥作用。
