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Pyocyanin Alters Redox Homeostasis and Carbon Flux through Central Metabolic Pathways in Pseudomonas aeruginosa PA14

Price-Whelan, Alexa and Dietrich, Lars E. P. and Newman, Dianne K. (2007) Pyocyanin Alters Redox Homeostasis and Carbon Flux through Central Metabolic Pathways in Pseudomonas aeruginosa PA14. Journal of Bacteriology, 189 (17). pp. 6372-6381. ISSN 0021-9193.

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The opportunistic pathogen Pseudomonas aeruginosa produces colorful, redox-active antibiotics called phenazines. Excretion of pyocyanin, the best-studied natural phenazine, is responsible for the bluish tint of sputum and pus associated with P. aeruginosa infections in humans. Although the toxicity of pyocyanin for other bacteria, as well as its role in eukaryotic infection, has been studied extensively, the physiological relevance of pyocyanin metabolism for the producing organism is not well understood. Pyocyanin reduction by P. aeruginosa PA14 is readily observed in standing liquid cultures that have consumed all of the oxygen in the medium. We investigated the physiological consequences of pyocyanin reduction by assaying intracellular concentrations of NADH and NAD+ in the wild-type strain and a mutant defective in phenazine production. We found that the mutant accumulated more NADH in stationary phase than the wild type. This increased accumulation correlated with a decrease in oxygen availability and was relieved by the addition of nitrate. Pyocyanin addition to a phenazine-null mutant also decreased intracellular NADH levels, suggesting that pyocyanin reduction facilitates redox balancing in the absence of other electron acceptors. Analysis of extracellular organic acids revealed that pyocyanin stimulated stationary-phase pyruvate excretion in P. aeruginosa PA14, indicating that pyocyanin may also influence the intracellular redox state by decreasing carbon flux through central metabolic pathways.

Item Type:Article
Newman, Dianne K.0000-0003-1647-1918
Additional Information:Copyright © 2007, American Society for Microbiology. Received 2 April 2007/ Accepted 15 May 2007. Published ahead of print on 25 May 2007. We acknowledge all of the members of the Newman laboratory, particularly Tracy K. Teal, for their technical advice and for comments and suggestions regarding the manuscript. This work was supported by NIH training grant 5T32GM07616 (to A.P.-W.), an EMBO long-term fellowship (to L.E.P.D.), and grants from the Packard Foundation and Howard Hughes Medical Institute (to D.K.N.). Supplemental material for this article may be found at
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Deposited On:22 Aug 2007
Last Modified:24 Oct 2017 15:06

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