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J. Bacteriol. doi:10.1128/JB.00075-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Cold Shock Exoribonuclease R (VacB) Is Involved in Aeromonas hydrophila Pathogenesis

Departments of Microbiology & Immunology, and Pathology, University of Texas Medical Branch, Galveston, TX 77555-1070, USA, Departments of Medical and Research Technology and Epidemiology and Preventive Medicine, University of Maryland, Baltimore, MD 21201, USA

^* To whom correspondence should be addressed. Email: achopra{at}utmb.edu.

	Abstract

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 an environmental isolate ATCC 7966^T of A. hydrophila and the vacB gene of Shigella flexneri. The A. hydrophila VacB protein contained 798 amino-acid residues with a molecular mass of 90.5 kDa and it 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. On the contrary, 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 a 2 LD₅₀ dose. On the other hand, the WT and complemented strains of A. hydrophila caused 80-90% 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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