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Updated: Oct 23, 2025

Quantifying Yersinia pseudotuberculosis Type III Secretion System Activity Following Iron Starvation and Anaerobic Growth
Published on: May 31, 2024
The Small Protein YmoA Controls the Csr System and Adjusts Expression of Virulence-Relevant Traits of Yersinia
Katja Böhme1, Ann Kathrin Heroven1, Stephanie Lobedann1
1Department of Molecular Infection Biology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Abstract:
Virulence gene expression of Yersinia pseudotuberculosis changes during the different stages of infection and this is tightly controlled by environmental cues. In this study, we show that the small protein YmoA, a member of the Hha family, is part of this process. It controls temperature- and nutrient-dependent early and later stage virulence genes in an opposing manner and co-regulates bacterial stress responses and metabolic functions. Our analysis further revealed that YmoA exerts this function by modulating the global post-transcriptional regulatory Csr system. YmoA pre-dominantly enhances the stability of the regulatory RNA CsrC. This involves a stabilizing stem-loop structure within the 5'-region of CsrC. YmoA-mediated CsrC stabilization depends on H-NS, but not on the RNA chaperone Hfq. YmoA-promoted reprogramming of the Csr system has severe consequences for the cell: we found that a mutant deficient of ymoA is strongly reduced in its ability to enter host cells and to disseminate to the Peyer's patches, mesenteric lymph nodes, liver and spleen in mice. We propose a model in which YmoA controls transition from the initial colonization phase in the intestine toward the host defense phase important for the long-term establishment of the infection in underlying tissues.
Insights
The small protein YmoA regulates virulence in Yersinia pseudotuberculosis by stabilizing the CsrC RNA, impacting bacterial stress and infection stages. A YmoA mutant shows reduced host cell entry and dissemination.
Area of Science:
- Microbiology
- Molecular Biology
- Pathogenesis
Background:
- Bacterial virulence gene expression is tightly regulated by environmental cues during infection.
- The small protein YmoA, belonging to the Hha family, is implicated in controlling virulence in Yersinia pseudotuberculosis.
Purpose of the Study:
- To elucidate the role of YmoA in regulating virulence gene expression, bacterial stress responses, and metabolic functions in Yersinia pseudotuberculosis.
- To investigate the mechanism by which YmoA modulates the Csr system and its impact on infection progression.
Main Methods:
- Analysis of YmoA's function in controlling temperature- and nutrient-dependent virulence genes.
- Investigation of YmoA's interaction with the Csr system, focusing on CsrC RNA stability.
- Assessment of a YmoA-deficient mutant's ability to infect host cells and disseminate in a mouse model.
Main Results:
- YmoA differentially controls early and late-stage virulence genes and co-regulates stress and metabolic functions.
- YmoA enhances CsrC RNA stability through a specific stem-loop structure, dependent on H-NS but not Hfq.
- A mutant lacking YmoA exhibited significantly reduced host cell invasion and dissemination to key organs (Peyer's patches, lymph nodes, liver, spleen) in mice.
Conclusions:
- YmoA acts as a key regulator of Yersinia pseudotuberculosis virulence by modulating the Csr system, specifically stabilizing CsrC RNA.
- YmoA is crucial for the transition from intestinal colonization to deeper tissue invasion, influencing the infection's establishment and severity.
- The findings propose a model where YmoA orchestrates the switch between initial colonization and host defense phases of infection.
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