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Journal of Bacteriology, September 2008, p. 5953-5962, Vol. 190, No. 17
0021-9193/08/$08.00+0     doi:10.1128/JB.00569-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Vibrio cholerae VciB Promotes Iron Uptake via Ferrous Iron Transporters{triangledown}

Alexandra R. Mey,* Elizabeth E. Wyckoff, Lindsey A. Hoover,{dagger} Carolyn R. Fisher, and Shelley M. Payne

Section of Molecular Genetics and Microbiology and Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas 78712-1095

Received 24 April 2008/ Accepted 18 June 2008

Vibrio cholerae uses a variety of strategies for obtaining iron in its diverse environments. In this study we report the identification of a novel iron utilization protein in V. cholerae, VciB. The vciB gene and its linked gene, vciA, were isolated in a screen for V. cholerae genes that permitted growth of an Escherichia coli siderophore mutant in low-iron medium. The vciAB operon encodes a predicted TonB-dependent outer membrane receptor, VciA, and a putative inner membrane protein, VciB. VciB, but not VciA, was required for growth stimulation of E. coli and Shigella flexneri strains in low-iron medium. Consistent with these findings, TonB was not needed for VciB-mediated growth. No growth enhancement was seen when vciB was expressed in an E. coli or S. flexneri strain defective for the ferrous iron transporter Feo. Supplying the E. coli feo mutant with a plasmid encoding either E. coli or V. cholerae Feo, or the S. flexneri ferrous iron transport system Sit, restored VciB-mediated growth; however, no stimulation was seen when either of the ferric uptake systems V. cholerae Fbp and Haemophilus influenzae Hit was expressed. These data indicate that VciB functions by promoting iron uptake via a ferrous, but not ferric, iron transport system. VciB-dependent iron accumulation via Feo was demonstrated directly in iron transport assays using radiolabeled iron. A V. cholerae vciB mutant did not exhibit any growth defects in either in vitro or in vivo assays, possibly due to the presence of other systems with overlapping functions in this pathogen.

* Corresponding author. Mailing address: The University of Texas at Austin, Section of Molecular Genetics and Microbiology, Austin, TX 78712-1095. Phone: (512) 471-5204. Fax: (512) 471-7088. E-mail: armey{at}mail.utexas.edu

{triangledown} Published ahead of print on 27 June 2008.

{dagger} Present address: Department of Biochemistry, The University of Wisconsin, Madison, WI 53706-1544.

Journal of Bacteriology, September 2008, p. 5953-5962, Vol. 190, No. 17
0021-9193/08/$08.00+0     doi:10.1128/JB.00569-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Fisher, C. R., Davies, N. M. L. L., Wyckoff, E. E., Feng, Z., Oaks, E. V., Payne, S. M. (2009). Genetics and Virulence Association of the Shigella flexneri Sit Iron Transport System. Infect. Immun. 77: 1992-1999 [Abstract] [Full Text]  


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