Extracytoplasmic-stress-responsive pathways modulate type III secretion in Yersinia pseudotuberculosis
Extracytoplasmic-stress-responsive pathways modulate type III secretion in Yersinia pseudotuberculosis
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DOI：
10.1128/iai.01346-06
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发表时间：
2007-08-01
影响因子：
3.1
通讯作者：
Francis, Matthew S.
中科院分区：
文献类型：
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作者：
Carlsson, Katrin E.;Liu, Junta;Francis, Matthew S.
三种信号转导途径，双组分系统CpxRA和BaeSR和替代的σ因子σ（E），响应于促进细菌适应变化的环境的细胞质外应激。至少CpxRA和sigma（E）途径控制蛋白质折叠和降解因子的产生，所述蛋白质折叠和降解因子对抗周质中蛋白质错误折叠的影响。这种功能还影响跨越细菌包膜的多组分细胞外附属物的生物发生，例如各种形式的皮利。在此，我们调查是否在肠道病原体假结核耶尔森氏菌的这些调节途径影响的Ysc-Yop III型分泌系统的功能。这是一种跨越细菌包膜的多组分分子注射器，用于将效应蛋白直接注射到真核细胞中。单个组分的破坏揭示了Cpx和sigma（E）途径对于Yops（耶尔森氏菌外部蛋白）的III型假结核耶尔森氏菌分泌是重要的。特别是，CpxA，传感器激酶的损失，降低了细菌膜中的结构Ysc（耶尔森氏菌分泌）组分的水平，这表明这些突变细菌不太能够组装功能性分泌装置。此外，这些细菌不再能够将Yops定位到真核细胞内部。此外，一个cpxA lcrQ双突变体工程过量生产和分泌Yops仍然受损的中毒细胞。因此，Cpx途径可能介导细菌-靶细胞接触的多种影响，从而调节耶尔森氏菌III型分泌依赖性宿主细胞毒性。
Three signal transduction pathways, the two-component systems CpxRA and BaeSR and the alternative sigma factor sigma(E), respond to extracytoplasmic stress that facilitates bacterial adaptation to changing environments. At least the CpxRA and sigma(E) pathways control the production of protein-folding and degradation factors that counter the effects of protein misfolding in the periplasm. This function also influences the biogenesis of multicomponent extracellular appendages that span the bacterial envelope, such as various forms of pili. Herein, we investigated whether any of these regulatory pathways in the enteropathogen Yersinia pseudotuberculosis affect the functionality of the Ysc-Yop type III secretion system. This is a multicomponent molecular syringe spanning the bacterial envelope used to inject effector proteins directly into eukaryotic cells. Disruption of individual components revealed that the Cpx and sigma(E) pathways are important for Y pseudotuberculosis type III secretion of Yops (Yersinia outer proteins). In particular, a loss of CpxA, a sensor kinase, reduced levels of structural Ysc (Yersinia secretion) components in bacterial membranes, suggesting that these mutant bacteria are less able to assemble a functional secretion apparatus. Moreover, these bacteria were no longer capable of localizing Yops into the eukaryotic cell interior. In addition, a cpxA lcrQ double mutant engineered to overproduce and secrete Yops was still impaired in intoxicating cells. Thus, the Cpx pathway might mediate multiple influences on bacterium-target cell contact that modulate Yersinia type III secretion-dependent host cell cytotoxicity.