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Journal of Bacteriology, November 2004, p. 7653-7658, Vol. 186, No. 22
0021-9193/04/$08.00+0 DOI: 10.1128/JB.186.22.7653-7658.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Department of Pharmacology, Case School of Medicine, Case Western Reserve University, Cleveland, Ohio
Received 8 June 2004/ Accepted 13 August 2004
corA encodes the constitutively expressed primary Mg2+ uptake system of most eubacteria and many archaea. Recently, a mutation in corA was reported to make Salmonella enterica serovar Typhimurium markedly resistant to Fe2+-mediated toxicity. Mechanistically, this was hypothesized to be from an ability of CorA to mediate the influx of Fe2+. Consequently, we directly examined Fe2+ transport and toxicity in wild-type versus corA cells. As determined by direct transport assay, CorA cannot transport Fe2+ and Fe2+ does not potently inhibit CorA transport of 63Ni2+. Mg2+ can, relatively weakly, inhibit Fe2+ uptake, but inhibition is not dependent on the presence of a functional corA allele. Although excess Fe2+ was slightly toxic to S. enterica serovar Typhimurium, we were unable to elicit a significant differential sensitivity in a wild-type versus a corA strain. We conclude that CorA does not transport Fe2+ and that the relationship, if any, between iron toxicity and corA is indirect.
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