This Article Full Text Full Text (PDF) Other Versions of this Article: JB.00075-08v1 190/10/3467    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Google Scholar Articles by Erova, T. E. Articles by Chopra, A. K. PubMed PubMed Citation Articles by Erova, T. E. Articles by Chopra, A. K.

 Previous Article  |  Next Article 

Journal of Bacteriology, May 2008, p. 3467-3474, Vol. 190, No. 10
0021-9193/08/$08.00+0     doi:10.1128/JB.00075-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

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

Departments of Microbiology and Immunology,¹ Pathology, University of Texas Medical Branch, Galveston, Texas 77555-1070,² Departments of Medical and Research Technology and Epidemiology and Preventive Medicine, University of Maryland, Baltimore, Maryland 21201³

Received 15 January 2008/ Accepted 6 March 2008

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 7966^T 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.

Published ahead of print on 14 March 2008.