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

SIMPLE SUMMARY: Understanding the underlying mechanisms of NH(4)(+) toxicity is essential for improving nitrogen use efficiency. Although numerous genes and factors have been identified to function in modulating the response to NH(4)(+) stress, NH(4)(+) toxicity remains poorly characterized. Our work reported here demonstrated a new role for CAP1 in shoot growth in response to NH(4)(+) stress. The enhanced sensitivity of the cap1-1 mutant to NH(4)(+) stress is linked with the role of CAP1 in regulation cell wall loosening and ROS accumulation. ABSTRACT: High levels of ammonium (NH(4)(+)) in soils inhibit plant growth and nitrogen utilization efficiency. Elucidating the underlying mechanisms of NH(4)(+) toxicity is essential for alleviating the growth inhibition caused by high NH(4)(+). Our previous work showed that [Ca(2+)](cyt)-associated protein kinase 1 (CAP1) regulates root hair growth in response to NH(4)(+) in Arabidopsis thaliana, and the cap1-1 mutant produces short root hairs under NH(4)(+) stress conditions. However, it is unclear whether CAP1 functions in other physiological processes in response to NH(4)(+). In the present study, we found that CAP1 also plays a role in attenuating NH(4)(+) toxicity to promote shoot growth. The cap1-1 mutant produced smaller shoots with smaller epidermal cells compared with the wild type in response to NH(4)(+) stress. Disruption of CAP1 enhanced the NH(4)(+)-mediated inhibition of the expression of cell enlargement-related genes. The cap1-1 mutant showed elevated reactive oxygen species (ROS) levels under NH(4)(+) 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(4)(+)-induced shoot growth inhibition by promoting cell wall extensibility and ROS homeostasis, thereby highlighting the role of CAP1 in the NH(4)(+) signal transduction pathway.