Characterization of the role of the SmpB-SsrA system in Yersinia pseudotuberculosis pathogenesis.

摘要

Pathogenic Yersinia has developed several strategies for successful infection. Yersinia utilizes a sophisticated type III secretion system to enhance its chances of survival and to overcome the host immune system. I 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, results showed that mutations in smpB-ssrA genes render the bacterium avirulent and unable to cause mortality in mice. Consistent with these observations, the mutant strain was unable to proliferate in macrophages and exhibited delayed Yop-mediated host cell cytotoxicity. Correspondingly, I provide evidences that the smpB-ssrA mutant suffers severe deficiencies in expression and secretion of Yersinia virulence effector proteins (Yops), 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. I also showed that YopH and YopM proteins are tagged by the SmpB-SsrA system, indicating a significant role for the system in expression of TTSS. These findings highlight the significance of the SmpB-SsrA system in bacterial pathogenesis, survival under adverse environmental conditions, and motility.