Okan Nihal A, Bliska James B, Karzai A Wali
Department of Biochemistry and Cell Biology, and Center for Infectious Diseases, Stony Brook University, Stony Brook, New York, USA.
PLoS Pathog. 2006 Jan;2(1):e6. doi: 10.1371/journal.ppat.0020006. Epub 2006 Jan 27.
Yersinia utilizes a sophisticated type III secretion system to enhance its chances of survival and to overcome the host immune system. SmpB (small protein B) and SsrA (small stable RNA A) are components of a unique bacterial translational control system that help maintain the bacterial translational machinery in a fully operational state. We have found that loss of the SmpB-SsrA function causes acute defects in the ability of Yersinia pseudotuberculosis to survive in hostile environments. Most significantly, we show that mutations in smpB-ssrA genes render the bacterium avirulent and unable to cause mortality in mice. Consistent with these observations, we show that the mutant strain is unable to proliferate in macrophages and exhibits delayed Yop-mediated host cell cytotoxicity. Correspondingly, we demonstrate that the smpB-ssrA mutant suffers severe deficiencies in expression and secretion of Yersinia virulence effector proteins, and that this defect is at the level of transcription. Of further interest is the finding that the SmpB-SsrA system might play a similar role in the related type III secretion system that governs flagella assembly and bacterial motility. These findings highlight the significance of the SmpB-SsrA system in bacterial pathogenesis, survival under adverse environmental conditions, and motility.
耶尔森氏菌利用一种复杂的III型分泌系统来提高其生存几率并克服宿主免疫系统。SmpB（小蛋白B）和SsrA（小稳定RNA A）是一种独特的细菌翻译控制系统的组成部分，该系统有助于使细菌翻译机制保持在完全运作的状态。我们发现，SmpB - SsrA功能的丧失会导致假结核耶尔森氏菌在恶劣环境中生存能力出现严重缺陷。最为显著的是，我们发现smpB - ssrA基因的突变会使该细菌失去毒性，无法在小鼠体内导致死亡。与这些观察结果一致的是，我们表明突变菌株无法在巨噬细胞中增殖，并表现出Yop介导的宿主细胞细胞毒性延迟。相应地，我们证明smpB - ssrA突变体在耶尔森氏菌毒力效应蛋白的表达和分泌方面存在严重缺陷，并且这种缺陷发生在转录水平。更有趣的是，有研究发现SmpB - SsrA系统可能在控制鞭毛组装和细菌运动的相关III型分泌系统中发挥类似作用。这些发现凸显了SmpB - SsrA系统在细菌致病机制、在不利环境条件下的生存以及运动性方面的重要性。
