Pseudomonas fluorescens orchestrates a fine metabolic-balancing act to counter aluminium toxicity
Article first published online: 25 MAR 2010
© 2010 Society for Applied Microbiology and Blackwell Publishing Ltd
Special Issue: Pseudomonas. Editors: Professors Burkhard Tummler, Victor de Lorenzo, Alain Filloux and Joyce Loper
Volume 12, Issue 6, pages 1384–1390, June 2010
How to Cite
Lemire, J., Mailloux, R., Auger, C., Whalen, D. and Appanna, V. D. (2010), Pseudomonas fluorescens orchestrates a fine metabolic-balancing act to counter aluminium toxicity. Environmental Microbiology, 12: 1384–1390. doi: 10.1111/j.1462-2920.2010.02200.x
- Issue published online: 3 JUN 2010
- Article first published online: 25 MAR 2010
- Received 7 November, 2009; accepted 15 January, 2010.
Aluminium (Al), an environmental toxin, is known to disrupt cellular functions by perturbing iron (Fe) homeostasis. However, Fe is essential for such metabolic processes as the tricarboxylic acid (TCA) cycle and oxidative phosphorylation, the two pivotal networks that mediate ATP production during aerobiosis. To counter the Fe conundrum induced by Al toxicity, Pseudomonas fluorescens utilizes isocitrate lyase and isocitrate dehydrogenase-NADP dependent to metabolize citrate when confronted with an ineffective aconitase provoked by Al stress. By invoking fumarase C, a hydratase devoid of Fe, this microbe is able to generate essential metabolites. To compensate for the severely diminished enzymes like Complex I, Complex II and Complex IV, the upregulation of a H2O-generating NADH oxidase enables the metabolism of citrate, the sole carbon source via a modified TCA cycle. The overexpression of succinyl-CoA synthetase affords an effective route to ATP production by substrate-level phosphorylation in the absence of O2. This fine metabolic balance enables P. fluorescens to survive the dearth of bioavailable Fe triggered by an Al environment, a feature that may have potential applications in bioremediation technologies.