Involvement of nitric oxide-mediated cytosolic glucose-6-phosphate dehydrogenase in soybean resistance to heavy metal toxicity.

Key message: Cytosolic G6PDH contributes to soybean tolerance to heavy metal exposure by alleviating oxidative damage, and in this process, nitric oxide may act upstream of cytosolic G6PDH. Heavy metal (HM) pollution in soil significantly impairs agricultural production and represents a substantial risk to food security. However, the underlying mechanism by which glucose-6-phosphate dehydrogenase (G6PDH or G6PD, EC 1.1.1.49) alleviates HM toxicity needs further clarification. In this study, the role of G6PDH in mitigating the toxicity of HMs (chromium, cadmium, copper, lead, and mercury) was examined in soybean (Glycine max L.) using pharmacological and transgenic approaches. The findings indicate that the enhanced G6PDH activity observed during HM exposure was attributable to cytosolic G6PDH induction. HM stress induced the expression of cytosolic G6PDH genes (GmG6PD6, GmG6PD7, and GmG6PD8), particularly GmG6PD7. Overexpression of GmG6PD7 in soybean hairy roots enhanced G6PDH activity and HM tolerance. The addition of a G6PDH inhibitor during HM exposure markedly reduced the levels of NADPH, ascorbic acid (ASA), and reduced glutathione (GSH) in soybean roots, thereby exacerbating oxidative damage. In contrast, overexpression of GmG6PD7 significantly increased the contents of NADPH, ASA, and GSH in transgenic soybean roots under HM exposure, thereby alleviating oxidative damage. Furthermore, nitric oxide (NO) stimulated an elevation in cytosolic G6PDH activity and GmG6PD7 expression under HM exposure. Notably, G6PDH demonstrated comparable functionality in response to all five HMs examined. In summary, the NO-mediated induction of cytosolic G6PDH enhances soybean resistance to HM exposure through strengthening the antioxidant defense system.