Is the maintenance of homeostatic mitochondrial signaling during stress a physiological role for alternative oxidase?
Article first published online: 21 MAY 2009
DOI: 10.1111/j.1399-3054.2009.01254.x
Copyright © Physiologia Plantarum 2009
Issue

Physiologia Plantarum
Special Issue: Alternative Oxidase
Volume 137, Issue 4, pages 392–406, December 2009
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How to Cite
Vanlerberghe, G. C., Cvetkovska, M. and Wang, J. (2009), Is the maintenance of homeostatic mitochondrial signaling during stress a physiological role for alternative oxidase?. Physiologia Plantarum, 137: 392–406. doi: 10.1111/j.1399-3054.2009.01254.x
Publication History
- Issue published online: 17 NOV 2009
- Article first published online: 21 MAY 2009
- Received 19 March 2009; revised 28 April 2009
- Abstract
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All plants maintain a non-energy-conserving pathway of mitochondrial electron transport referred to as alternative oxidase (AOX) respiration. Here, we briefly review some of the most prevailing themes for the metabolic and physiological roles of this respiratory pathway. Many of these themes relate to the potential of AOX to provide metabolic homeostasis in response to fluctuating cellular conditions, such as is often seen during stress. We then review reverse genetic experiments that have been used to test these hypotheses. To date, such experiments have been limited to just two dicot species and have only targeted one member (a stress-induced member) of the AOX multigene family. Nonetheless, the experiments to date strongly reinforce the idea that AOX respiration is of particular importance during abiotic and biotic stress. Finally, we propose that another core role of AOX may be to modulate the strength of a stress-signaling pathway from the mitochondrion that controls cellular responses to stress. In this way, AOX could be acting to provide a degree of signaling homeostasis from the mitochondrion. This hypothesis may provide explanation for some of the disparate results seen in reverse genetic experiments regarding the impact of AOX on the reactive oxygen network and oxidative damage.

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