Genetic relationships between the G protein beta gamma complex, Ste5p, Ste20p and Cdc42p: investigation of effector roles in the yeast pheromone response pathway.

Genetic relationships between the G protein beta gamma complex, Ste5p, Ste20p and Cdc42p: investigation of effector roles in the yeast pheromone response pathway.
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G 蛋白 beta gamma 复合物、Ste5p、Ste20p 和 Cdc42p 之间的遗传关系:酵母信息素响应途径中效应器作用的研究。

DOI:
10.1093/genetics/143.1.103
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发表时间:
1996
期刊:
影响因子:
3.3
通讯作者:
Kurjan,J
Kurjan,J
中科院分区:
生物学2区
文献类型:
--
作者:
Akada,R;Kallal,L;Johnson,DI;Kurjan,J

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酵母菌aeG蛋白βγ二聚体(Ste 4p/Ste 18 p)位于Gpalp亚基的下游,激活信息素反应途径,因此必须与下游效应物相互作用。合成不育突变体加剧表型的ste 4-t突变被分离出来,以确定蛋白质的功能与Ste 4p相互作用。astel 8突变体的鉴定表明,该筛选可以鉴定与Ste 4p直接相互作用的蛋白。其他的突变发生在STE 5和STE 20激酶基因上,它们在途径中作用于靠近STE 4p的位置,还有一个新的基因叫做STE 21。STE 20无效突变体显示出残余交配,表明另一种激酶可能提供某些功能。半乳糖控制下的Ste 5 p的过表达激活了信息素反应途径。这种激活依赖于Ste 4p和Ste 18 p,部分依赖于Ste 20 p。这些结果不能用Ste 4p → Ste 20 p → Ste 5 p的线性途径来解释。Cdc 42 p的过表达导致报告基因的信息素诱导略有增加,并且Cdc 42 p的活化形式的过表达导致进一步增加两倍。信息素反应途径组分的突变并不能抑制与活化的CDC 42突变相关的致死性,这表明这种效应不依赖于信息素反应途径。
TheSaccharomyces cerevisiaeG protein βγ dimer, Ste4p/Ste18p, acts downstream of theasubunit, Gpalp, to activate the pheromone response pathway and therefore must interact with a downstream effector. Synthetic sterile mutants that exacerbate the phenotype ofste4-tsmutations were isolated to identify proteins that functionally interact with Ste4p. The identification of astel8mutant indicated that this screen could identify proteins that interact directly with Ste4p. The other mutations were inSTE5and theSTE20kinase gene, which act near Ste4p in the pathway, and a new gene calledSTE21. ste20null mutants showed residual mating, suggesting that another kinase may provide some function. Overexpression of Ste5p under galactose control activated the pheromone response pathway. This activation was dependent on Ste4p and Ste18p and partially dependent on Ste20p. These results cannot be explained by the linear pathway of Ste4p → Ste20p → Ste5p. Overexpression of Cdc42p resulted in a slight increase in pheromone induction of a reporter gene, and overexpression of activated forms of Cdc42p resulted in a further twofold increase. Mutations in pheromone response pathway components did not suppress the lethality associated with the activatedCDC42mutations, suggesting that this effect is independent of the pheromone response pathway.
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