Open AccessThe V ibrio parahaemolyticus effector VopC mediates C dc42‐dependent invasion of cultured cells but is not required for pathogenicity in an animal model of infection
Author(s) -
Okada Ryu,
Zhou Xiaohui,
Hiyoshi Hirotaka,
Matsuda Shigeaki,
Chen Xiang,
Akeda Yukihiro,
Kashimoto Takashige,
Davis Brigid M.,
Iida Tetsuya,
Waldor Matthew K.,
Kodama Toshio
Publication year - 2014
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12252
Subject(s) - vibrio parahaemolyticus , biology , virulence , effector , internalization , microbiology and biotechnology , secretion , rhoa , type three secretion system , rac1 , cdc42 , gtpase , cell , bacteria , signal transduction , gene , biochemistry , genetics
Summary V ibrio parahaemolyticus is a G ram‐negative marine bacterium that causes acute gastroenteritis in humans. The virulence of V . parahaemolyticus is dependent upon a type III secretion system ( T 3 SS 2). One effector for T 3 SS 2, VopC , is a homologue of the catalytic domain of cytotoxic necrotizing factor ( CNF ), and was recently reported to be a R ho family GTP ase activator and to be linked to internalization of V . parahaemolyticus by non‐phagocytic cultured cells. Here, we provide direct evidence that VopC deamidates R ac1 and CDC 42, but not RhoA , in vivo . Our results alsosuggest that VopC , through its activation of R ac1, contributes to formation of actin stress fibres in infected cells. Invasion of host cells, which occurs at a low frequency, does not seem linked to R ac1 activation, but instead appears to require CDC 42. Finally, using an infant rabbit model of V . parahaemolyticus infection, we show that the virulence of V . parahaemolyticus is not dependent upon VopC ‐mediated invasion. Genetic inactivation of VopC did not impair intestinal colonization nor reduce signs of disease, including fluid accumulation, diarrhoea and tissue destruction. Thus, although VopC can promote host cell invasion, such internalization is not a critical step of the disease process, consistent with the traditional view of V . parahaemolyticus as an extracellular pathogen.