Defects in protein glycosylation cause SHO1-dependent activation of a STE12 signaling pathway in yeast.
Defects in protein glycosylation cause SHO1-dependent activation of a STE12 signaling pathway in yeast.
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发表时间：
2000-07
期刊：
影响因子：
3.3
通讯作者：
Paul J Cullen;Janet Schultz;J. Horecka;Brian J. Stevenson;Y. Jigami;George F. Sprague
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文献类型：
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作者：
Paul J Cullen;Janet Schultz;J. Horecka;Brian J. Stevenson;Y. Jigami;George F. Sprague
在单倍体酿酒酵母中，交配通过激活信息素反应途径发生。对激活该途径的突变体的遗传选择发现了一类细胞壁完整性缺陷的突变体。PGI 1、PMI 40、PSA 1、DPM 1、ALG 1、MNN 10、SPT 14和OCH 1的部分功能丧失等位基因（甘露糖利用和蛋白糖基化所需的基因）在缺乏基础信号（ste 4）的细胞中激活了信息素反应途径依赖性报告基因（FUS 1）。通过向己糖异构酶突变体pgi 1 -101和pmi 40 -101中添加甘露糖来抑制途径活化，这绕过了这些突变体中甘露糖生物合成的要求。在dpm 1 -101突变体中，途径激活也被含有产生Dpm 1底物的RER 2或PSA 1的质粒抑制。在甘露糖利用/蛋白质糖基化突变体中FUS 1转录的激活需要来自三种不同信号通路的一些但不是全部蛋白质：信息素响应、侵入性生长和HOG通路。我们特别提出Sho 1--> Ste 20/Ste 50--> Ste 11--> Ste 7--> Kss 1--> Ste 12通路负责这些突变体中FUS 1转录的激活。由于信息素反应途径组分的损失导致甘露糖利用/蛋白质糖基化突变体的合成生长缺陷，我们认为Sho 1-> Ste 12途径有助于维持营养细胞的细胞壁完整性。
In haploid Saccharomyces cerevisiae, mating occurs by activation of the pheromone response pathway. A genetic selection for mutants that activate this pathway uncovered a class of mutants defective in cell wall integrity. Partial loss-of-function alleles of PGI1, PMI40, PSA1, DPM1, ALG1, MNN10, SPT14, and OCH1, genes required for mannose utilization and protein glycosylation, activated a pheromone-response-pathway-dependent reporter (FUS1) in cells lacking a basal signal (ste4). Pathway activation was suppressed by the addition of mannose to hexose isomerase mutants pgi1-101 and pmi40-101, which bypassed the requirement for mannose biosynthesis in these mutants. Pathway activation was also suppressed in dpm1-101 mutants by plasmids that contained RER2 or PSA1, which produce the substrates for Dpm1. Activation of FUS1 transcription in the mannose utilization/protein glycosylation mutants required some but not all proteins from three different signaling pathways: the pheromone response, invasive growth, and HOG pathways. We specifically suggest that a Sho1 --> Ste20/Ste50 --> Ste11 --> Ste7 --> Kss1 --> Ste12 pathway is responsible for activation of FUS1 transcription in these mutants. Because loss of pheromone response pathway components leads to a synthetic growth defect in mannose utilization/protein glycosylation mutants, we suggest that the Sho1 --> Ste12 pathway contributes to maintenance of cell wall integrity in vegetative cells.