ToxR of Vibrio cholerae affects biofilm, rugosity and survival with Acanthamoeba castellanii
1 Karolinska Institute, Department of Laboratory Medicine, Division of Clinical Microbiology, Karolinska University Hospital, Huddinge, SE-141 86, Stockholm, Sweden
2 Department of Molecular Biology, Umeå University, 90187 Umeå, Sweden
BMC Research Notes 2012, 5:33 doi:10.1186/1756-0500-5-33Published: 16 January 2012
Vibrio cholerae causes the diarrheal disease cholera and utilizes different survival strategies in aquatic environments. V. cholerae can survive as free-living or in association with zooplankton and can build biofilm and rugose colonies. The bacterium expresses cholera toxin (CT) and toxin-coregulated pilus (TCP) as the main virulence factors. These factors are co-regulated by a transcriptional regulator ToxR, which modulates expression of outer membrane proteins (OmpU) and (OmpT). The aims of this study were to disclose the role of ToxR in expression of OmpU and OmpT, biofilm and rugose colony formation as well as in association with the free-living amoeba Acanthamoeba castellanii at different temperatures.
The toxR mutant V. cholerae produced OmpT, significant biofilm and rugose colonies compared to the wild type that produced OmpU, decreased biofilm and did not form rugoes colonies at 30°C. Interestingly, neither the wild type nor toxR mutant strain could form rugose colonies in association with the amoebae. However, during the association with the amoebae it was observed that A. castellanii enhanced survival of V. cholerae wild type compared to toxR mutant strain at 37°C.
ToxR does seem to play some regulatory role in the OmpT/OmpU expression shift, the changes in biofilm, rugosity and survival with A. castellanii, suggesting a new role for this regulatory protein in the environments.