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Updated: Aug 10, 2026

Analysis of Yersinia enterocolitica Effector Translocation into Host Cells Using Beta-lactamase Effector Fusions
Published on: October 13, 2015
A Role for the SmpB-SsrA system in Yersinia pseudotuberculosis pathogenesis
Nihal A Okan1, James B Bliska, A Wali Karzai
1Department of Biochemistry and Cell Biology, and Center for Infectious Diseases, Stony Brook University, Stony Brook, New York, USA.
The SmpB-SsrA system is crucial for Yersinia pseudotuberculosis virulence and survival. Loss of this system prevents infection and mortality in mice by impairing essential virulence factors.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Molecular Biology
Background:
- Yersinia employs a type III secretion system (T3SS) for immune evasion and survival.
- The SmpB-SsrA system regulates bacterial translation and maintains cellular function.
- The role of SmpB-SsrA in Yersinia pathogenesis was previously unclear.
Purpose of the Study:
- To investigate the function of the SmpB-SsrA system in Yersinia pseudotuberculosis.
- To determine the impact of SmpB-SsrA on bacterial virulence, survival, and T3SS activity.
- To explore potential roles of SmpB-SsrA in other bacterial systems.
Main Methods:
- Generating smpB-ssrA mutant strains of Yersinia pseudotuberculosis.
- Assessing bacterial survival in vitro and in vivo (murine model).
- Quantifying bacterial proliferation, cytotoxicity, and Yop effector protein expression/secretion.
Main Results:
- Loss of SmpB-SsrA function severely impairs Yersinia pseudotuberculosis survival in hostile environments.
- Mutations in smpB-ssrA render the bacterium avirulent, causing no mortality in mice.
- The smpB-ssrA mutant shows defective proliferation in macrophages, delayed cytotoxicity, and significantly reduced Yop expression/secretion at the transcriptional level.
- The SmpB-SsrA system may also influence flagellar assembly and motility.
Conclusions:
- The SmpB-SsrA system is essential for Yersinia virulence and pathogenesis.
- SmpB-SsrA plays a critical role in regulating bacterial survival, T3SS function, and virulence factor expression.
- This system is a potential target for therapeutic intervention against Yersinia infections.
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