REK1通过磷酸化RBOHD来调节活性氧稳态，从而在拟南芥中正向调控盐胁迫响应。

Abstract

Salinity induces the accumulation of reactive oxygen species (ROS) in plants, thereby regulating plant growth and development, including seed germination. However, the molecular mechanisms underlying the regulation of ROS homeostasis in response to salt stress remain largely unknown. Here, we showed that an leucine‐rich‐repeat receptor‐like kinase, REK1, regulates ROS production by phosphorylating the NADPH oxidase respiratory burst oxidase homolog D (RBOHD) in Arabidopsis in response to salt stress. Salt‐induced ROS accumulates extensively in rek1 mutants, causing stress that reduces the seed germination rate of rek1 below that of the wild‐type (Col‐0), resulting in the salt‐sensitive phenotype. Furthermore, REK1 interacts with RBOHD and phosphorylates it at Ser163, thereby regulating its NADPH oxidase activity and influencing ROS production under salt stress. Genetic data revealed that the salt‐sensitive phenotype of rek1 is rescued in rek1 rbohd mutants. In summary, our study revealed a salt stress regulation mechanism that modulates ROS production in Arabidopsis through the REK1‐RBOHD pathway. The study shows that REK1, a member of the leucine‐rich repeat receptor‐like kinase family, increases plant tolerance to salt stress during seed germination by phosphorylating NADPH oxidase respiratory burst oxidase homolog D, thereby regulating its oxidase activity and reactive oxygen species levels.