REGULATION OF THE YEAST PHEROMONE RESPONSE PATHWAY BY G-PROTEIN SUBUNITS
REGULATION OF THE YEAST PHEROMONE RESPONSE PATHWAY BY G-PROTEIN SUBUNITS
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DOI：
10.1002/j.1460-2075.1990.tb08161.x
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发表时间：
1990-03-01
期刊：
影响因子：
11.4
通讯作者：
MATSUMOTO, K
中科院分区：
文献类型：
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作者：
NOMOTO, S;NAKAYAMA, N;MATSUMOTO, K
酵母的GPA1、STE4和STE18基因分别编码与。α同源的蛋白。度量。并可以利用。哺乳动物G蛋白复合物的亚基，似乎介导对交配信息素的反应。半乳糖诱导的GAL1启动子过度表达STE4蛋白，激活信息素反应通路，导致细胞周期阻滞在G1期晚期，诱导FUS1基因表达，从而抑制无受体突变体delta .ste2的不育性。反过来，STE18的破坏抑制了STE4过表达诱导的信息素反应的激活，这表明STE18产物是STE4作用所必需的。然而，在STE18野生型存在的情况下，STE4和STE18蛋白的过表达并不比STE4的过表达产生更强的信息素反应。这些结果表明。亚基是信息素反应的限制成分支持。并可以利用。亚基起正向调节作用。此外，GPA1过表达可阻止STE4过表达介导的细胞周期阻滞，但不能阻止FUS1诱导。这意味着。亚基可能通过与。β相互作用而起负调节作用。并可以利用。交配信息素信号通路中的亚基。
The yeast GPA1, STE4, and STE18 genes encode proteins homologous to the respective .alpha., .beta. and .gamma. subunits of the mammalian G protein complex which appears to mediate the response to mating pheromones. Over expression of the STE4 protein by the galactose-inducible GAL1 promoter caused activation of the pheromone response pathway which resulted in cell-cycle arrest in late G1 phase and induction of the FUS1 gene expression, thereby suppressing the sterility of the receptor-less mutant .DELTA.ste2. Disruption of STE18, in turn, suppressed activation of the pheromone response induced by overexpression of STE4, suggesting that the STE18 product is required for the STE4 action. However, overexpression of both the STE4 and STE18 proteins did not generate a stronger pheromone response than overexpression of STE4 in the presence of wild-type levels of STE18. These results suggest that the .beta. subunit is the limiting component for the pheromone response and support the idea that .beta. and .gamma. subunit act as a positive regulator. Furthermore, overexpression of GPA1 prevented cell-cycle arrested but not FUS1 induction mediated by overexpression of STE4. This implies that the .alpha. subunit acts as a negative regulator presumably through interacting with .beta. and .gamma. subunits in the mating pheromone signaling pathway.