Redox-regulation of mitochondrial metabolism through thioredoxin o1 facilitates light induction of photosynthesis.

Despite the well-known biochemistry of the major pathways involved in central carbon and amino acid metabolism, there are still gaps regarding their regulation or regulatory interactions. Recent research demonstrated the physiological significance of the mitochondrial redox machinery, particularly thioredoxin o1 (TRXo1), for proper regulation of the tricarboxylic acid cycle, components of the mitochondrial electron transport chain and photorespiration. These findings imply that TRXo1 regulation contributes to the metabolic acclimation toward changes in the prevailing environmental conditions. Here, we analyzed if TRXo1 is involved in the light induction of photosynthesis. Our results show that the mutant activates CO assimilation rates to a significantly lower extend than wild type in response to short-term light/dark changes. Metabolite analysis suggests that activation of glycine-to-serine conversion catalyzed through glycine decarboxylase in conjunction with serine hydroxymethyltransferase in is slowed down at onset of illumination. We propose that redox regulation via TRXo1 is necessary to allow the rapid induction of mitochondrial steps of the photorespiratory cycle and, in turn, to facilitate light-induction of photosynthesis.