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首页> 外文期刊>Infection and immunity >SseK1 and SseK2 Are Novel Translocated Proteins of Salmonella enterica Serovar Typhimurium
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SseK1 and SseK2 Are Novel Translocated Proteins of Salmonella enterica Serovar Typhimurium

机译：SseK1和SseK2是肠沙门氏菌鼠伤寒沙门氏菌的新型易位蛋白。

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Salmonella enterica is a gram-negative, facultative intracellular pathogen that causes disease symptoms ranging from gastroenteritis to typhoid fever. A key virulence strategy is the translocation of bacterial effector proteins into the host cell, mediated by the type III secretion systems (TTSSs) encoded in Salmonella pathogenicity island 1 (SPI-1) and SPI-2. In S. enterica serovar Typhimurium LT2, we identified the protein products of STM4157 and STM2137 as novel candidate secreted proteins by comparison to known secreted proteins from enterohemorrhagic Escherichia coli and Citrobacter rodentium. The STM4157 and STM2137 proteins, which we have designated SseK1 and SseK2, respectively, are 61% identical at the amino acid level and differ mainly in their N termini. Western analysis showed that in vitro accumulation and secretion of these proteins in serovar Typhimurium were affected by mutations in the two-component systems SsrA/B and PhoP/Q, which are key mediators of intracellular growth and survival. SPI-2 TTSS-dependent translocation of recombinant SseK1::Cya was evident at 9 h postinfection of epithelial cells, while translocation of SseK2::Cya was not detected until 21 h. Remarkably, the translocation signal for SseK1 was contained within the N-terminal 32 amino acids. Fractionation of infected epithelial cells revealed that following translocation SseK1 localizes to the host cytosol, which is unusual among the currently known Salmonella effectors. Phenotypic analysis of ΔsseK1, ΔsseK2, and ΔsseK1/ΔsseK2 mutants provided evidence for a role that was not critical during systemic infection. In summary, this work demonstrates that SseK1 and SseK2 are novel translocated proteins of serovar Typhimurium.
机译：沙门氏菌是一种革兰氏阴性，兼性细胞内病原体，可引起从胃肠炎到伤寒的各种疾病症状。关键的毒力策略是细菌效应蛋白转运到宿主细胞中，由沙门氏菌致病岛1（SPI-1）和SPI-2编码的III型分泌系统（TTSS）介导。在 S中。肠炎血清型鼠伤寒LT2，通过与肠出血性肠出血性大肠杆菌已知分泌蛋白的比较，我们确定了 STM4157 和 STM2137 的蛋白质产物和啮齿类柠檬酸杆菌。我们分别命名为SseK1和SseK2的STM4157和STM2137蛋白在氨基酸水平上具有61％的同一性，主要区别在于它们的N末端。西方分析表明，鼠伤寒血清中这些蛋白的体外积累和分泌受到两个组分系统SsrA / B和PhoP / Q突变的影响，这是细胞内生长和存活的关键介质。重组SseK1 :: Cya的SPI-2 TTSS依赖性易位在上皮细胞感染后9 h明显，而直到21 h才检测到SseK2 :: Cya的易位。值得注意的是，SseK1的易位信号包含在N端32个氨基酸内。被感染的上皮细胞的分离显示，SseK1易位后定位在宿主细胞质中，这在当前已知的 Salmonella 效应子中并不常见。 Δ sseK1 ，Δ sseK2 和Δ sseK1 /Δ sseK2 突变体的表型分析提供了以下证据在全身感染期间并不​​重要。总之，这项工作证明SseK1和SseK2是鼠伤寒沙门氏菌的新型易位蛋白。

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