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J Bacteriol, February 1998, p. 762-765, Vol. 180, No. 3
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

A Functional Homolog of Escherichia coli NhaR in Vibrio cholerae

S. G. Williams,^1,* O. Carmel-Harel,² and P. A. Manning¹

Microbial Pathogenesis Unit, Department of Microbiology and Immunology, University of Adelaide, Adelaide, South Australia 5005, Australia,¹ and Division of Microbial and Molecular Ecology, Institute of Life Sciences, Hadassah Medical School, Hebrew University of Jerusalem, 91904 Jerusalem, Israel²

Received 28 August 1997/Accepted 4 December 1997

Escherichia coli NhaR controls expression of a sodium/proton (Na⁺/H⁺) antiporter, NhaA. The Vibrio cholerae NhaR protein shows over 60% identity to those of Escherichia coli and Salmonella enteritidis. V. cholerae NhaR complements an E. coli nhaR mutant for growth in 100 mM LiCl-33 mM NaCl, pH 7.6, and enhances the Na⁺-dependent induction of an E. coli chromosomal nhaA::lacZ fusion. These findings indicate functional homology to E. coli NhaR. Two V. cholerae nhaR mutants were constructed by using kanamycin resistance cartridge insertion at different sites to disrupt the gene. Both mutants showed sensitivity to growth in 120 mM LiCl, pH 9.2, compared with the wild-type strain and could be complemented by the introduction of V. cholerae nhaR on a low-copy-number plasmid. An nhaR mutation had no detectable effect on the virulence of the V. cholerae strain in the infant mouse model, suggesting that the antiporter system involved is not required in vivo, at least in this animal model.

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^* Corresponding author. Mailing address: Microbial Pathogenesis Unit, Department of Microbiology and Immunology, University of Adelaide, Adelaide, South Australia 5005, Australia. Phone: (618) 83033266. Fax: (618) 83034362. E-mail: swilliam{at}microb.adelaide.edu.au.

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