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Updated: Aug 14, 2026

A Non-Coding Small RNA MicC Contributes to Virulence in Outer Membrane Proteins in Salmonella Enteritidis
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A Non-Coding Small RNA MicC Contributes to Virulence in Outer Membrane Proteins in Salmonella Enteritidis

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Negative regulation of Salmonella pathogenicity island 2 is required for contextual control of virulence during

Brian K Coombes1, Mark E Wickham, Michael J Lowden

  • 1Michael Smith Laboratories, Department of Microbiology and Immunology, University of British Columbia, Vancouver, BC, Canada V6T 1Z4.

Proceedings of the National Academy of Sciences of the United States of America
|November 23, 2005
PubMed

Insights

Researchers identified YdgT as a key regulator of Salmonella pathogenicity island-2 (SPI-2). Proper control of SPI-2 by YdgT is essential for Salmonella virulence during systemic infection.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Molecular Biology

Background:

  • Salmonella enterica uses the type III secretion system (SPI-2) for intracellular survival and replication within macrophages.
  • SPI-2 virulence gene expression is induced upon macrophage entry, but its precise regulation in vivo, especially negative control, is not fully understood.

Purpose of the Study:

  • To identify and characterize negative regulators of the Salmonella pathogenicity island-2 (SPI-2) virulence system.
  • To elucidate the role of YdgT in modulating SPI-2 gene expression and its impact on Salmonella pathogenesis.

Main Methods:

  • Genetic characterization of YdgT as a negative modulator of SPI-2.
  • In vivo competitive infection models to assess the virulence phenotype of ydgT mutants.
  • Analysis of SPI-2 gene expression and bacterial pathogenesis.

Main Results:

  • YdgT was identified as a negative regulator of the SPI-2 pathogenicity island.
  • ydgT mutants exhibited a biphasic virulence phenotype: initial gain-of-virulence followed by attenuation.
  • Overexpression of SPI-2 virulence genes in ydgT mutants led to reduced systemic pathogenesis.

Conclusions:

  • YdgT-mediated negative regulation of SPI-2 is crucial for Salmonella systemic pathogenesis.
  • Precise, contextual control of SPI-2 by YdgT is necessary for full virulence during infection.
  • Dysregulation and overexpression of SPI-2 virulence factors can be detrimental to bacterial pathogenesis in vivo.

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