Modeling the effects of prl mutations on the Escherichia coli SecY complex
Modeling the effects of prl mutations on the Escherichia coli SecY complex
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DOI：
10.1128/jb.187.18.6454-6465.2005
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发表时间：
2005-09-01
影响因子：
3.2
通讯作者：
Flower, AM
中科院分区：
文献类型：
--
作者：
Smith, MA;Clemons, WM;Flower, AM
负责蛋白质跨细菌膜转运的装置是保守的SecY复合物，它由SecY、SecE和SecG组成。先前的遗传学分析为蛋白质输出机制以及组成蛋白之间的相互作用提供了见解。特别是secE和secY的prl抑制等位基因，它们能使具有缺陷信号序列的分泌蛋白输出，已被证明特别有用。在此，我们报道了secE和secY中新型突变的分离，以及prl突变组合的表型效应。根据最近发表的古细菌SecY复合物的晶体结构，对这些新的等位基因以及先前已鉴定的prl突变进行了分析。我们的结果支持并扩展了一个Prl抑制活性模型，该模型提出所有的prlA和prlG等位基因要么使通道的关闭状态不稳定，要么使开放形式稳定。因此，这些突变体使得通道能够在没有野生型复合物所要求的信号序列结合这一触发事件的情况下开放。
The apparatus responsible for translocation of proteins across bacterial membranes is the conserved SecY complex, consisting of SecY, SecE, and SecG. Prior genetic analysis provided insight into the mechanisms of protein export, as well as the interactions between the component proteins. In particular, the prl suppressor alleles of secE and secY, which allow export of secretory proteins with defective signal sequences, have proven particularly useful. Here, we report the isolation of novel mutations in secE and secY, as well as the phenotypic effects of combinations of prl mutations. These new alleles, as well as previously characterized prl mutations, were analyzed in light of the recently published crystal structure of the archacal SecY complex. Our results support and expand a model of Prl suppressor activity that proposes that all of the prlA and prlG alleles either destabilize the closed state of the channel or stabilize the open form. These mutants thus allow channel opening to occur without the triggering event of signal sequence binding that is required in a wild-type complex.