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VopV, an F-actin-binding type III secretion effector, is required for Vibrio parahaemolyticus-induced enterotoxicity

Hirotaka Hiyoshi1, Toshio Kodama, Kazunobu Saito

  • 1Laboratory of Genomic Research on Pathogenic Bacteria, International Research Center for Infectious Diseases, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan.

Cell Host & Microbe
|October 25, 2011
PubMed

Insights

Researchers identified VopV as a key effector protein responsible for the enterotoxicity of Vibrio parahaemolyticus via its type III secretion system 2 (T3SS2). VopV targets F-actin, crucial for bacterial virulence.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Molecular Biology

Background:

  • Vibrio parahaemolyticus causes human gastroenteritis and possesses two type III secretion systems (T3SS1 and T3SS2).
  • T3SS2 is essential for the bacterium's enterotoxicity, but the specific effector proteins remain unidentified.

Purpose of the Study:

  • To identify the critical effector(s) of Vibrio parahaemolyticus T3SS2 responsible for enterotoxicity.
  • To elucidate the mechanism by which T3SS2 mediates bacterial virulence.

Main Methods:

  • Genetic analysis to identify effector proteins.
  • Biochemical assays to determine protein function, including F-actin binding.
  • Investigating homologous genes and secretion systems in related bacterial species.

Main Results:

  • VopV was identified as a crucial effector for T3SS2-dependent enterotoxicity in V. parahaemolyticus.
  • VopV exhibits F-actin binding activity, and its enterotoxicity correlates with this binding.
  • A homologous vopV gene and a T3SS2-related system contribute to the enterotoxicity of a non-O1/non-O139 Vibrio cholerae strain.

Conclusions:

  • VopV is a key F-actin-targeting effector involved in the enterotoxicity mediated by T3SS2.
  • The findings highlight VopV's role in the pathogenesis of T3SS2-possessing bacterial pathogens.
  • This study provides insights into the molecular mechanisms of Vibrio-associated gastroenteritis.

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