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.

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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