Abstract

Redox state in plant mitochondria is a key factor regulating metabolism of the plant cell and generating signalling cascades in response to abiotic and biotic stress, light regime, and cell differentiation. While the NAD pool plays primarily role in energy production, the internal mitochondrial NADP pool, which represents 20–25 % of the NAD pool, is important for the regulation of metabolic processes associated with mitochondria. The reduction level of NADP is the main factor regulating via thioredoxin the activities of several enzymes of the tricarboxylic acid cycle, the alternative oxidase, and other proteins. The NADPH/NADP+ ratio in the matrix is controlled by NADP-dependent isocitrate dehydrogenase, by the non-proton-translocating transhydrogenase reaction, and by the oxidation via Ca2+-dependent NADPH dehydrogenase. The mitochondrial redox state regulates the transport in and out of the organelle, balancing redox reactions in other compartments. This is achieved, in particular, via the operation of malate and citrate valves. The efflux of citrate provides the carbon skeletons for transamination and for ammonia refixation during photorespiration. The consequence of an increased redox state of NAD(H) and NADP(H) pools in mitochondria is the formation of reactive oxygen species, via leakage of electrons from the electron transport chain, and of NO, by using nitrite as an alternative electron acceptor under oxygen deficiency. It is concluded that the mitochondrial redox state is a central regulator of plant metabolism and a trigger of signalling cascades in response to stress and during plant development.

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