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Cold Shock Exoribonuclease R (VacB) is Involved in Aeromonas hydrophila Pathogenesis
Citation:
Erova, T. E., V. G. Kosykh, A. A. Fadl, J. Sha, A. J. Horneman, AND A. K. Chopra. Cold Shock Exoribonuclease R (VacB) is Involved in Aeromonas hydrophila Pathogenesis. JOURNAL OF BACTERIOLOGY. American Society for Microbiology, Washington, DC, 190(10):3467-3474, (2008).
Impact/Purpose:
Explore and support the best approaches for determining how, when, and for what pathogens, VFAR concepts can be used to identify pathogens that are hazardous to humans, in order to identify pathogens to nominate for the CCL process.
Description:
In this study, we cloned and sequenced a virulence-associated gene (vacB) from a clinical isolate SSU of Aeromonas hydrophila. We identified this gene based on our recently annotated genome sequence of the environmental isolate ATCC 7966T of A. hydrophila and the vacB gene of Shigella flexneri. The A. hydrophila VacB protein contained 798 amino acid residues, had a molecular mass of 90.5 kDa, and exhibited an exoribonuclease (RNase R) activity. The RNase R of A. hydrophila was a cold-shock protein and was required for bacterial growth at low temperature. The vacB isogenic mutant, which we developed by homologous recombination using marker exchange mutagenesis, was unable to grow at 4°C. In contrast, the wild-type (WT) A. hydrophila exhibited significant growth at this low temperature. Importantly, the vacB mutant was not defective in growth at 37°C. The vacB mutant also exhibited reduced motility, and these growth and motility phenotype defects were restored after complementation of the vacB mutant. The A. hydrophila RNase R-lacking strain was found to be less virulent in a mouse lethality model (70% survival) when given by the intraperitoneal route at as two 50% lethal doses (LD50). On the other hand, the WT and complemented strains of A. hydrophila caused 80 to 90% of the mice to succumb to infection at the same LD50 dose. Overall, this is the first report demonstrating the role of RNase R in modulating the expression of A. hydrophila virulence.
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