Stefan C J, Blumer K J
Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110.
Mol Cell Biol. 1994 May;14(5):3339-49. doi: 10.1128/mcb.14.5.3339-3349.1994.
To identify functional domains of G-protein-coupled receptors that control pathway activation, ligand discrimination, and receptor regulation, we have used as a model the alpha-factor receptor (STE2 gene product) of the yeast Saccharomyces cerevisiae. From a collection of random mutations introduced in the region coding for the third cytoplasmic loop of Ste2p, six ste2sst alleles were identified by genetic screening methods that increased alpha-factor sensitivity 2.5- to 15-fold. The phenotypic effects of ste2sst and sst2 mutations were not additive, consistent with models in which the third cytoplasmic loop of the alpha-factor receptor and the regulatory protein Sst2p control related aspects of pheromone response and/or desensitization. Four ste2sst mutations did not dramatically alter cell surface expression or agonist binding affinity of the receptor; however, they did permit detectable responses to an alpha-factor antagonist. One ste2sst allele increased receptor binding affinity for alpha-factor and elicited stronger responses to antagonist. Results of competition binding experiments indicated that wild-type and representative mutant receptors bound antagonist with similar affinities. The antagonist-responsive phenotypes caused by ste2sst alleles were therefore due to defects in the ability of receptors to discriminate between agonist and antagonist peptides. One ste2sst mutation caused rapid, ligand-independent internalization of the receptor. These results demonstrate that the third cytoplasmic loop of the alpha-factor receptor is a multifunctional regulatory domain that controls pathway activation and/or desensitization and influences the processes of receptor activation, ligand discrimination, and internalization.
为了确定控制信号通路激活、配体识别和受体调节的G蛋白偶联受体的功能结构域,我们使用酿酒酵母的α因子受体(STE2基因产物)作为模型。从在编码Ste2p第三胞质环的区域引入的一系列随机突变中,通过遗传筛选方法鉴定出六个ste2sst等位基因,这些等位基因使α因子敏感性提高了2.5至15倍。ste2sst和sst2突变的表型效应不是累加的,这与α因子受体的第三胞质环和调节蛋白Sst2p控制信息素反应和/或脱敏相关方面的模型一致。四个ste2sst突变没有显著改变受体的细胞表面表达或激动剂结合亲和力;然而,它们确实允许对α因子拮抗剂产生可检测的反应。一个ste2sst等位基因增加了受体对α因子的结合亲和力,并引发了对拮抗剂更强的反应。竞争结合实验结果表明,野生型和代表性突变体受体以相似的亲和力结合拮抗剂。因此,ste2sst等位基因引起的拮抗剂反应表型是由于受体区分激动剂和拮抗剂肽的能力存在缺陷。一个ste2sst突变导致受体快速、配体非依赖性内化。这些结果表明,α因子受体的第三胞质环是一个多功能调节结构域,它控制信号通路激活和/或脱敏,并影响受体激活、配体识别和内化过程。