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Journal of Bacteriology, March 2004, p. 1409-1414, Vol. 186, No. 5
0021-9193/04/$08.00+0 DOI: 10.1128/JB.186.5.1409-1414.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Department of Biological Sciences, Dartmouth College, Hanover, New Hampshire 03755,1 Pfizer Co., Ann Arbor, Michigan 481052
Received 13 August 2003/ Accepted 14 November 2003
In many bacteria, the ferric uptake regulator (Fur) protein plays a central role in the regulation of iron uptake genes. Because iron figures prominently in the agriculturally important symbiosis between soybean and its nitrogen-fixing endosymbiont Bradyrhizobium japonicum, we wanted to assess the role of Fur in the interaction. We identified a fur mutant by selecting for manganese resistance. Manganese interacts with the Fur protein and represses iron uptake genes. In the presence of high levels of manganese, bacteria with a wild-type copy of the fur gene repress iron uptake systems and starve for iron, whereas fur mutants fail to repress iron uptake systems and survive. The B. japonicum fur mutant, as expected, fails to repress iron-regulated outer membrane proteins in the presence of iron. Unexpectedly, a wild-type copy of the fur gene cannot complement the fur mutant. Expression of the fur mutant allele in wild-type cells leads to a fur phenotype. Unlike a B. japonicum fur-null mutant, the strain carrying the dominant-negative fur mutation is unable to form functional, nitrogen-fixing nodules on soybean, mung bean, or cowpea, suggesting a role for a Fur-regulated protein or proteins in the symbiosis.
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