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Journal of Bacteriology, November 2007, p. 7774-7781, Vol. 189, No. 21
0021-9193/07/$08.00+0     doi:10.1128/JB.00962-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Cobalt Targets Multiple Metabolic Processes in Salmonella enterica{triangledown}

Michael P. Thorgersen and Diana M. Downs*

Department of Bacteriology, University of Wisconsin—Madison, Madison, Wisconsin 53706

Received 18 June 2007/ Accepted 12 August 2007

Cobalt is essential for growth of Salmonella enterica and other organisms, yet this metal can be toxic when present in excess. Wild-type Salmonella exhibits several metabolic defects when grown in the presence of cobalt, some of which generate visible growth consequences. Work herein identifies sulfur assimilation, iron homeostasis, and Fe-S cluster metabolism as targets for cobalt toxicity. In each case it is proposed that cobalt exerts its effect by one of two mechanisms: direct competition with iron or indirectly through a mechanism that involves the status of reduced thiols in the cell. Cobalt toxicity results in decreased siroheme production, increased expression of the Fur regulon, and decreased activity of Fe-S cluster proteins. The consequences of reduced sulfite reductase activity in particular are exacerbated by the need for glutathione in cobalt resistance. Significantly, independent metabolic perturbations could be detected at cobalt concentrations below those required to generate a detectable growth defect.

* Corresponding author. Mailing address: Department of Bacteriology, University of Wisconsin—Madison, 1550 Linden Dr., Madison, WI 53706. Phone: (608) 238-0383. Fax: (608) 262-9865. E-mail: downs{at}bact.wisc.edu

{triangledown} Published ahead of print on 24 August 2007.

Journal of Bacteriology, November 2007, p. 7774-7781, Vol. 189, No. 21
0021-9193/07/$08.00+0     doi:10.1128/JB.00962-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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