The mechanism of exogenous gibberellin A3 protecting sorghum shoots from S-metolachlor Phytotoxicity

BACKGROUND S-metolachlor (MET) was used to prevent weed infestation in sorghum fields, but inappropriate application could result in phytotoxicity on sorghum. Exogenous gibberellin A(3) (GA(3)) has been applied for alleviating the phytotoxicity of MET. However, its detoxification mechanism is still not well known. RESULTS Leaf deformity of sorghum caused by 200 mg/L MET was alleviated by treating sorghum shoots with 800 mg/L GA(3), and the injury recovery rate of growth index was over 73%. More importantly, GA(3) could not accelerate the metabolic rate of MET in sorghum. The result of phytohormone metabolomics showed that endogenous GA(3) content in sorghum decreased by 78.10% with MET treatment, while abscisic acid (ABA) content increased by 120.2%, resulting in 10.3-fold increase of ABA/GA(3) ratio. Content of ABA and GA(3) increased by 11.9- and 21.1-fold with MET and GA(3) treatment, respectively, leading to ABA/GA(3) ratio restoration. Moreover, MET inhibited the expression of genes encoding key enzymes related to GA synthesis including CPS1, KO2, KAO, GA20ox1D and ABA8ox gene related to ABA metabolism. The transcription levels of GA metabolism-related genes CYP714D1 and GA2ox were up-regulated by 11.2- and 7.2-fold, while ABA synthesis-related genes NCED and ZEP were up-regulated by 8.0- and 3.0-fold, respectively, with MET and GA(3) treatment. Conclusion In this study, exogenous GA(3) protecting sorghum shoots from MET phytotoxicity was due to supplement the MET-induced GA(3) deficiency by absorbing exogenous GA(3), and restore homeostasis of ABA and GA(3) by promoting ABA synthesis, which provides novel insights for mechanism of GA(3) alleviating MET phytotoxicity. (c) 2022 Society of Chemical Industry.

Automated summary

The study found that exogenous gibberellin A(3) (GA(3)) can alleviate the phytotoxicity of S-metolachlor (MET) on sorghum. GA(3) alleviated the MET-induced deficiency of GA(3) by absorbing exogenous GA(3), and restored the homeostasis of abscisic acid (ABA) and GA(3) by promoting ABA synthesis.