Is the maintenance of homeostatic mitochondrial signaling during stress a physiological role for alternative oxidase?

Authors

  • Greg C. Vanlerberghe,

    Corresponding author
    1. Department of Biological Sciences, University of Toronto Scarborough, 1265 Military Trail, Toronto, Ontario, Canada M1C 1A4
    2. Department of Cell and Systems Biology, University of Toronto, 25 Harbord St., Toronto, Ontario, Canada M5S3G5
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  • Marina Cvetkovska,

    1. Department of Biological Sciences, University of Toronto Scarborough, 1265 Military Trail, Toronto, Ontario, Canada M1C 1A4
    2. Department of Cell and Systems Biology, University of Toronto, 25 Harbord St., Toronto, Ontario, Canada M5S3G5
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  • Jia Wang

    1. Department of Biological Sciences, University of Toronto Scarborough, 1265 Military Trail, Toronto, Ontario, Canada M1C 1A4
    2. Department of Cell and Systems Biology, University of Toronto, 25 Harbord St., Toronto, Ontario, Canada M5S3G5
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e-mail: gregv@utsc.utoronto.ca

Abstract

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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