Journal of Bacteriology, January 2001, p. 483-489, Vol. 183, No. 2
0021-9193/01/$04.00+0 DOI: 10.1128/JB.183.2.483-489.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
andDepartment of Microbiology and Immunology, East Carolina University School of Medicine, Greenville, North Carolina 27858-4354,1 and Department of Microbiology, University of Minnesota, Minneapolis, Minnesota 55455-03122
Received 24 August 2000/Accepted 27 October 2000
Genetic and biochemical studies have established that Fur and iron mediate repression of Bordetella alcaligin siderophore system (alc) genes under iron-replete nutritional growth conditions. In this study, transcriptional analyses using Bordetella chromosomal alc-lacZ operon fusions determined that maximal alc gene transcriptional activity under iron starvation stress conditions is dependent on the presence of alcaligin siderophore. Mutational analysis and genetic complementation confirmed that alcaligin-responsive transcriptional activation of Bordetella alcaligin system genes is dependent on AlcR, a Fur-regulated AraC-like positive transcriptional regulator encoded within the alcaligin gene cluster. AlcR-mediated transcriptional activation is remarkably sensitive to inducer, occurring at extremely low alcaligin concentrations. This positive autogenous control circuit involving alcaligin siderophore as the inducer for AlcR-mediated transcriptional activation of alcaligin siderophore biosynthesis and transport genes coordinates environmental and intracellular signals for maximal expression of these genes under conditions in which the presence of alcaligin in the environment is perceived.
Present address: Department of Biology, Washington University,
Saint Louis, MO 63130-4899.
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