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Infect. Immun. doi:10.1128/IAI.01704-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Vibrio parahaemolyticus inhibition of Rho-family GTPase activation requires a functional chromosome I type three secretion system

Department of Microbiology and Infectious Diseases, University of Calgary

^* To whom correspondence should be addressed. Email: rdevinne{at}ucalgary.ca.

	Abstract

Vibrio parahaemolyticus is a leading cause of seafood borne gastroenteritis, however its virulence mechanisms are not well understood. The identification of type three secreted proteins has provided candidate virulence factors whose functions are still being elucidated. Genotypic strain variability contributes a level of complexity to understanding the role of different virulence factors. The ability of V. parahaemolyticus to inhibit Rho-family GTPases and cause cytoskeletal disruption was examined in HeLa cells. After infection of HeLa cells, intracellular Rho activation was inhibited in response to external stimuli. In vitro activation of Rho, Rac, and Cdc42 isolated from infected HeLa cell lysates was also inhibited, indicating that the bacteria were specifically targeting GTPase activation. Inhibition of Rho-family GTPase activation was retained for clinical and environmental isolates of V. parahaemolyticus, and was dependent on a functional chromosome I type three secretion system (CI-T3SS). GTPase inhibition was independent of haemolytic toxin genotype and the chromosome II (CII) T3SS. Rho inhibition was accompanied by a shift in the total actin pool to its monomeric form. These phenotypes were abrogated in a mutant strain lacking the CI-T3S effector Vp1686, suggesting that inhibiting actin polymerization may be a downstream effect of Vp1686-dependent GTPase inhibition. Although Vp1686 has been previously characterized as a potential virulence factor in macrophages, our findings reveal an effect on cultured HeLa cells. The ability to inhibit Rho-family GTPases independently of the CII-T3SS and the haemolytic toxins may provide insight into the mechanisms of virulence used by strains lacking these virulence factors.