Mutational analysis of SEC4 suggests a cyclical mechanism for the regulation of vesicular traffic.
Mutational analysis of SEC4 suggests a cyclical mechanism for the regulation of vesicular traffic.
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SEC4 的突变分析表明了调节囊泡交通的循环机制。
DOI：
10.1002/j.1460-2075.1989.tb03560.x
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Novick,PJ
中科院分区：
文献类型：
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作者：
Walworth,NC;Goud,B;Kabcenell,AK;Novick,PJ
SEC 4是酵母分泌的最后阶段所需的必需基因，其突变等位基因已通过体外诱变产生。蛋白质C端两个半胱氨酸残基的缺失导致可溶性非功能蛋白，表明这两个残基是Sec 4p正常定位于分泌囊泡和质膜所必需的。正如预测的那样，产生的SEC 4突变等位基因模拟H-ras的活化转化等位基因，不结合GTP。在含有野生型SEC 4的细胞中该等位基因的存在导致分泌缺陷和分泌囊泡的积累。遗传研究结果表明，该等位基因的行为是一种显性功能丧失突变体，因此会阻止野生型蛋白质正常发挥功能。我们提出了一个模型，其中Sec 4p周期之间的活动和非活动状态，以介导的融合囊泡的质膜。
Mutant alleles of SEC4, an essential gene required for the final stage of secretion in yeast, have been generated by in vitro mutagenesis. Deletion of the two cysteine residues at the C terminus of the protein results in a soluble non‐functional protein, indicating that those two residues are required for normal localization of Sec4p to secretory vesicles and the plasma membrane. A mutant allele of SEC4 generated to mimic an activated, transforming allele of H‐ras, as predicted, does not bind GTP. The presence of this allele in cells containing wild‐type SEC4 causes a secretory defect and the accumulation of secretory vesicles. The results of genetic studies indicate that this allele behaves as a dominant loss of function mutant and as such prevents wild‐type protein from functioning properly. We propose a model in which Sec4p cycles between an active and an inactive state in order to mediate the fusion of vesicles to the plasma membrane.