Singlet oxygen-induced signalling depends on the metabolic status of the Chlamydomonas reinhardtii cell
La signalisation induite par l'oxygène singulet dépend de l'état métabolique de la cellule de Chlamydomonas reinhardtii
Résumé
Using a mutant screen, we identified trehalose 6-phosphate phosphatase 1 (TSPP1) as a functional enzyme dephosphorylating trehalose 6-phosphate (Tre6P) to trehalose in Chlamydomonas reinhardtii. The tspp1 knockout results in reprogramming of the cell metabolism via altered transcriptome. As a secondary effect, tspp1 also shows impairment in $^1O_2$-induced chloroplast retrograde signalling. From transcriptomic analysis and metabolite profiling, we conclude that accumulation or deficiency of certain metabolites directly affect $^1O_2$-signalling. $^1O_2$-inducible GLUTATHIONE PEROXIDASE 5 (GPX5) gene expression is suppressed by increased content of fumarate and 2-oxoglutarate, intermediates in the tricarboxylic acid cycle (TCA cycle) in mitochondria and dicarboxylate metabolism in the cytosol, but also myo-inositol, involved in inositol phosphate metabolism and phosphatidylinositol signalling system. Application of another TCA cycle intermediate, aconitate, recovers $^1O_2$-signalling and GPX5 expression in otherwise aconitate-deficient tspp1. Genes encoding known essential components of chloroplast-to-nucleus $^1O_2$-signalling, PSBP2, MBS, and SAK1, show decreased transcript levels in tspp1, which also can be rescued by exogenous application of aconitate. We demonstrate that chloroplast retrograde signalling involving 1 O 2 depends on mitochondrial and cytosolic processes and that the metabolic status of the cell determines the response to $^1O_2$ .
Domaines
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Licence |
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