Identification of early nuclear target genes of plastidial redox signals that trigger the long-term response of Arabidopsis to light quality shifts

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Dietzel, Lars | Glässer, Christine | Liebers, Monique | Hiekel, Stefan | Courtois, Florence | Czarnecki, Olaf | Schlicke, Hagen | Zubo, Yan | Börner, Thomas | Mayer, Klaus | Grimm, Bernhard | Pfannschmidt, Thomas

Edité par CCSD ; Springer Verlag (Germany) -

International audience. Natural illumination conditions are highly variable and because of their sessile life style plantsare forced to acclimate to them at cellular and molecular level. Changes in light intensity orquality induce changes in the reduction/oxidation (redox) state of the photosynthetic electronchain that act as trigger for compensatory acclimation responses comprising functional andstructural adjustments of photosynthesis and metabolism. Such responses include redoxcontrolledchanges in plant gene expression in nucleus and organelles. Here we describe astrategy for the identification of early redox-regulated genes (ERGs) in the nucleus of themodel organism Arabidopsis thaliana which significantly respond 30 or 60 min after thegeneration of a reduction signal in the photosynthetic electron transport chain. By comparingthe response of wild-type plants with that of the acclimation mutant stn7 we could specificallyidentify ERGs. The results reveal a significant impact of chloroplast redox signals on distinctnuclear gene groups including genes for the mitochondrial electron transport chain,tetrapyrrole biosynthesis, carbohydrate metabolism and signalling lipid synthesis. Theseexpression profiles are clearly different from that observed in response to reduction of thephotosynthetic electron transport (PET) by high light treatments. The identified ERGs, thus,are unique to redox imbalances in PET and were used for the analysis of potential redoxresponsivecis-elements, trans-factors and chromosomal regulatory hot spots. The dataidentify a novel redox-responsive element and indicate extensive redox control attranscriptional and chromosomal levels that point to an unprecedented impact of redox signalson epigenetic processes.

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