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| Antioxidant metabolism and redox signalling in plant mitochondria and their relationship to plant defence |
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Christine H Foyer
Crop Performance and Improvement, Rothamsted Research, Harpenden, Herts AL5 2JQ, UK
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Mitochondria have not traditionally been regarded as a major source of active oxygen species (AOS) in leaves. Indeed, in C3 plants in the light, peroxisomal and chloroplastic H2O2 production is likely up to 30-100 times faster than formation of H2O2 in the mitochondria. Nevertheless, the mitochondrial oxidative load could be crucial in influencing and setting the cellular redox-stat. Like other compartments of the plant cell, mitochondria house both enzymic and non-enzymic antioxidants, and are the site of ascorbic acid biosynthesis. The final step of ascorbic acid biosynthesis is located in the inner mitochondrial membrane and recent results suggest that respiratory electron flow may control ascorbate synthesis. The molecular signature of ascorbate deficiency in the Arabidopsis thaliana vtc1 mutant will be described. Of the 171 genes that are differentially expressed in vtc1 compared to the wild type, many are involved in plant defence. Furthermore, transcript changes indicate that growth and development are constrained in vtc1 by modulation of the balance between abscisic acid (ABA) and gibberellic acid (GA) signalling.
In agreement, ABA is significantly higher in vtc1 than the wild type and spraying with GA results in comparable increases in growth in the two genotypes. Incubating vtc1 leaf discs in ascorbate can reverse key features of the molecular signature of ascorbate deficiency. High ascorbate modified the abundance of 495 transcripts including genes involved in plant defence. Evidence will be provided to show that ascorbate is involved in metabolic cross-talk between redox-regulated pathways. The importance of the mitochondrial electron transport chain in controlling oxidative stress in plant cells will be considered. The Nicotiana sylvestris mutant, CMSII, lacks functional complex I and has hence lost of a major NADH sink. The implications for cellular redox balance will be discussed in terms of the substantial re-adjustments in antioxidant defence that are observed in the mutant. Perturbed complex I function initiates signalling which resets the antoxidative capacity throughout the cell, evidenced by modified expression of mitochondrial antioxidants (alternative oxidase and Mn-SOD) but also of chloroplastic Fe-SOD, peroxisomal catalase, and cytosolic APX. This remote signalling acts to lower cellular H2O2 and allows soluble cellular antioxidants (ascorbate, glutathione) to retain a high reduction state. Thus, localised redox balance in the mitochondria may be extremely important as a signal that determines everyday cell death and survival.
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