4.4 Article

Transcriptional activation of Bordetella alcaligin siderophore genes requires the AlcR regulator with alcaligin as inducer

Journal

JOURNAL OF BACTERIOLOGY
Volume 183, Issue 2, Pages 483-489

Publisher

AMER SOC MICROBIOLOGY
DOI: 10.1128/JB.183.2.483-489.2001

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Funding

  1. NIAID NIH HHS [R01 AI031088, AI-31088, R21 AI031088] Funding Source: Medline
  2. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI031088, R29AI031088, R21AI031088] Funding Source: NIH RePORTER

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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 ale 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.

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