The amelioration of cadmium (Cd2+) toxicity in plants by ammonium (NH4+) has been widely investigated. However, the molecular mechanisms underpinning this amelioration have remained ambiguous. Here, we found that NH4+ significantly reduces Cd2+ accumulation and enhances antioxidant capacity by increasing ABA accumulation, which, in turn, improves Cd2+ tolerance in rice seedlings. A combination of qPCR, yeast-one-hybrid and dual-luciferase assays, and CUT&RUN-qPCR methods demonstrates that OsbZIP20 directly binds to the promoters of OsAPX2 and OsCATA, activating their transcription, and we show that the process requires phosphorylation modification of OsbZIP20 by OsSAPK9. Under Cd2+ stress, Osbzip20 and Ossapk9 mutants show reduced peroxidase and catalase activities, higher H2O2 accumulation, and reduced Cd2+ tolerance. In sum, our results elucidate a novel mechanism by which NH4+ enhances Cd2+ resistance, through ABA-SAPK9-bZIP20-APX2/CATA, offering a new strategy for improving Cd2+ resistance in rice.

中文翻译：

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铵态氮通过以 ABA 依赖性方式激活水稻幼苗中的 bZIP20-APX2/CATA 转录模块来减轻镉毒性


铵态氮 （NH4+） 对植物中镉 （Cd2+） 的毒性已得到广泛研究。然而，支撑这种改善的分子机制仍然模棱两可。在这里，我们发现 NH4+ 通过增加 ABA 积累显着减少 Cd2+ 积累并增强抗氧化能力，进而提高水稻幼苗对 Cd2+ 的耐受性。qPCR、酵母单杂交和双荧光素酶测定以及 CUT&RUN-qPCR 方法的组合表明，OsbZIP20 直接与 OsAPX2 和 OsCATA 的启动子结合，激活它们的转录，我们表明该过程需要 OsSAPK9 对 OsbZIP20 的磷酸化修饰。在 Cd2+ 胁迫下，Osbzip20 和 Ossapk9 突变体表现出过氧化物酶和过氧化氢酶活性降低、H2O2 积累增加和 Cd2+ 耐受性降低。总之，我们的结果阐明了 NH4+ 通过 ABA-SAPK9-bZIP20-APX2/CATA 增强 Cd2+ 抗性的新机制，为提高水稻 Cd2+ 抗性提供了一种新策略。