This study aimed to reveal the mechanistic basis of the melatonin‐mediated amelioration of salinity stress in plants. Electrophysiological experiments revealed that melatonin decreased salt‐induced K⁺ efflux (a critical determinant of plant salt tolerance) in a dose‐ and time‐dependent manner and reduced sensitivity of the plasma membrane K⁺‐permeable channels to hydroxyl radicals. These beneficial effects of melatonin were abolished by NADPH oxidase blocker DPI. Transcriptome analyses revealed that melatonin induced 585 (448 up‐ and 137 down‐regulated) and 59 (54 up‐ and 5 down‐regulated) differentially expressed genes (DEGs) in the root tip and mature zone, respectively. The most noticeable changes in the root tip were melatonin‐induced increase in the expression of several DEGs encoding respiratory burst NADPH oxidases (OsRBOHA and OsRBOHF), calcineurin B‐like/calcineurin B‐like‐interacting protein kinase (OsCBL/OsCIPK), and calcium‐dependent protein kinase (OsCDPK) under salt stress. Melatonin also enhanced the expression of potassium transporter genes (OsAKT1, OsHAK1, and OsHAK5). Taken together, these results indicate that melatonin improves salt tolerance in rice by enabling K⁺ retention in roots, and that the latter process is conferred by melatonin scavenging of hydroxyl radicals and a concurrent OsRBOHF‐dependent ROS signalling required to activate stress‐responsive genes and increase the expression of K⁺ uptake transporters in the root tip.

中文翻译：

---

褪黑素通过依赖NADPH氧化酶的质膜K +转运蛋白和K +稳态来改善水稻盐胁迫的耐性。

这项研究旨在揭示褪黑素介导的植物盐分胁迫改善的机理基础。电生理实验揭示褪黑激素降低盐诱导ķ ⁺在质膜K的剂量和时间依赖性的方式和降低的灵敏度外排（临界植物耐盐性决定簇）⁺羟基自由基的渗透通道。NADPH氧化酶阻滞剂DPI消除了褪黑激素的这些有益作用。转录组分析显示，褪黑素分别在根尖和成熟区诱导585个（上调448个，下调137个）和59个（54个上调和5个下调）差异表达基因（DEG）。根尖最明显的变化是褪黑激素诱导的几种编码呼吸爆发NADPH氧化酶的DEG（OsRBOHA和OsRBOHF），钙调神经磷酸酶B样/钙调神经磷酸酶B样相互作用蛋白激酶（OsCBL / OsCIPK）的表达增加，以及钙依赖蛋白激酶（OsCDPK）在盐胁迫下。褪黑激素还增强了钾转运蛋白基因（OsAKT1，OsHAK1和OsHAK5）的表达。综上所述，这些结果表明褪黑激素通过使K ⁺保留在根中而提高了水稻的耐盐性，而后者的过程是通过褪黑激素清除羟基自由基和同时激活激活应激反应基因和依赖OsRBOHF的ROS信号传导而实现的。增加根尖中K ⁺吸收转运蛋白的表达。