FtsH-dependent degradation of phage shock protein C in Yersinia enterocolitica and Escherichia coli.
FtsH-dependent degradation of phage shock protein C in Yersinia enterocolitica and Escherichia coli.
复制标题
小肠结肠炎耶尔森菌和大肠杆菌中噬菌体休克蛋白 C 的 FtsH 依赖性降解。
DOI：
10.1128/jb.05942-11
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发表时间：
2011
影响因子：
3.2
通讯作者：
Darwin,AndrewJ
中科院分区：
文献类型：
--
作者：
Singh,Sindhoora;Darwin,AndrewJ
在大肠杆菌和小肠结肠炎耶尔森氏菌中广泛保守的噬菌体休克蛋白（Psp）胞质外应激反应已被广泛研究。这两个物种都有PspF、-A、-B和-C蛋白，它们与包括Y在内的强大表型有关。小肠结肠炎毒力PspB和PspC是细胞质膜蛋白，在外膜分泌素蛋白的错误定位过程中，它们是psp基因表达的胁迫依赖性诱导和细菌存活所必需的。此前，我们报道了Y。小肠结肠炎菌PspB的功能是通过未表征的转录后机制积极控制PspC的量。在这项研究中，我们发现，细胞质膜蛋白酶FtsH参与了这一现象。FtsH使Y. PspC与其结合伴侣PspB的共产生足以防止这种不稳定。相比之下，FtsH没有影响Psp系统的任何其他核心组件。这些数据表明，未复合的PspC可能是特别有害的细菌细胞和FtsH作为一个重要的质量控制机制，以消除it. This的观察，PspC生产所造成的毒性降低，无论是通过共同生产的PspB或增加合成的FtsH支持。我们还发现FtsH依赖的PspC失稳现象在Y. enterocolitica和E.杆菌
The widely conserved phage shock protein (Psp) extracytoplasmic stress response has been studied extensively in Escherichia coli and Yersinia enterocolitica. Both species have the PspF, -A, -B, and -C proteins, which have been linked to robust phenotypes, including Y. enterocolitica virulence. PspB and PspC are cytoplasmic membrane proteins required for stress-dependent induction ofpspgene expression and for bacterial survival during the mislocalization of outer membrane secretin proteins. Previously, we reported that Y. enterocolitica PspB functions to positively control the amount of PspC by an uncharacterized posttranscriptional mechanism. In this study, we have discovered that the cytoplasmic membrane protease FtsH is involved in this phenomenon. FtsH destabilizes PspC in Y. enterocolitica, but coproduction of PspC with its binding partner PspB was sufficient to prevent this destabilization. In contrast, FtsH did not affect any other core component of the Psp system. These data suggested that uncomplexed PspC might be particularly deleterious to the bacterial cell and that FtsH acts as an important quality control mechanism to remove it. This was supported by the observation that toxicity caused by PspC production was reduced either by coproduction of PspB or by increased synthesis of FtsH. We also found that the phenomenon of FtsH-dependent PspC destabilization is conserved between Y. enterocolitica and E. coli.