The Receptor-like Kinase CAP1 Promotes Shoot Growth under Ammonium Stress.

High levels of ammonium (NH) in soils inhibit plant growth and nitrogen utilization efficiency. Elucidating the underlying mechanisms of NH toxicity is essential for alleviating the growth inhibition caused by high NH. Our previous work showed that [Ca]-associated protein kinase 1 (CAP1) regulates root hair growth in response to NH in , and the mutant produces short root hairs under NH stress conditions. However, it is unclear whether CAP1 functions in other physiological processes in response to NH. In the present study, we found that CAP1 also plays a role in attenuating NH toxicity to promote shoot growth. The mutant produced smaller shoots with smaller epidermal cells compared with the wild type in response to NH stress. Disruption of CAP1 enhanced the NH-mediated inhibition of the expression of cell enlargement-related genes. The mutant showed elevated reactive oxygen species (ROS) levels under NH stress, as well as increased expression of respiratory burst oxidase homologue genes and decreased expression of catalase genes compared with the wild type. Our data reveal that CAP1 attenuates NH-induced shoot growth inhibition by promoting cell wall extensibility and ROS homeostasis, thereby highlighting the role of CAP1 in the NH signal transduction pathway.