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The presence of pesticide residues in fresh fruits and vegetables poses a serious threat to human health. Brassinosteroids (BRs) can reduce pesticide residues in plants, but the underlying mechanisms still remain unclear. Here, we identified a tomato glutaredoxin gene GRXS25 which was induced by 24-epibrassinolide (EBR) and chlorothalonil (CHT) in a way dependent on apoplastic reactive oxygen species (ROS). Silencing of GRXS25 in tomato abolished EBR-induced glutathione S-transferases (GSTs) gene expression and activity, leading to an increased CHT residue. Yeast two-hybrid and bimolecular fluorescence complementation assays showed protein-protein interaction between GRXS25 and a transcription factor TGA2. Electrophoretic mobility shift and chromatin immunoprecipitation assays indicated that TGA2 factor bound to the TGACG-motif in the GST3 promoter. While silencing of TGA2 strongly compromised, overexpression of TGA2 enhanced expression of GST genes and CHT residue metabolism. Our results suggest that BR-induced apoplastic ROS trigger metabolism of pesticide residue in tomato plants through activating TGA2 factor via GRXS25-dependent posttranslational redox modification. Activation of plant detoxification through physiological approaches has potential implication in improving the food safety of agricultural products.
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•The glutaredoxin GRXS25 is essential for BR-induced chlorothalonil metabolism.•Induction of GRXS25 expression is dependent on RBOH1-mediated ROS.•GRXS25 interacts with the TGA2 transcription factor.•TGA2 factor regulates detoxification genes through binding to the TGACG-motif.•GRXS25 and TGA2 factor mediate BR-induced chlorothalonil metabolism.
Apoplastic H2O2, glutaredoxin GRXS25 and TGA2 factor constitute a signaling module that mediates brassinosteroid-induced chlorothalonil metabolism in tomato.