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Journal of Bacteriology, March 2007, p. 2101-2109, Vol. 189, No. 5
0021-9193/07/$08.00+0     doi:10.1128/JB.01377-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Disruption of sitA Compromises Sinorhizobium meliloti for Manganese Uptake Required for Protection against Oxidative Stress{triangledown}

Bryan W. Davies and Graham C. Walker*

Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139

Received 29 August 2006/ Accepted 8 December 2006

During the initial stages of symbiosis with the host plant Medicago sativa, Sinorhizobium meliloti must overcome an oxidative burst produced by the plant in order for proper symbiotic development to continue. While identifying mutants defective in symbiosis and oxidative stress defense, we isolated a mutant with a transposon insertion mutation of sitA, which encodes the periplasmic binding protein of the putative iron/manganese ABC transporter SitABCD. Disruption of sitA causes elevated sensitivity to the reactive oxygen species hydrogen peroxide and superoxide. Disruption of sitA leads to elevated catalase activity and a severe decrease in superoxide dismutase B (SodB) activity and protein level. The decrease in SodB level strongly correlates with the superoxide sensitivity of the sitA mutant. We demonstrate that all free-living phenotypes of the sitA mutant can be rescued by the addition of exogenous manganese but not iron, a result that strongly implies that SitABCD plays an important role in manganese uptake in S. meliloti.

* Corresponding author. Mailing address: Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139. Phone: (617) 253-6711. Fax: (617) 253-2643. E-mail: gwalker{at}mit.edu.

{triangledown} Published ahead of print on 15 December 2006.

Journal of Bacteriology, March 2007, p. 2101-2109, Vol. 189, No. 5
0021-9193/07/$08.00+0     doi:10.1128/JB.01377-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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