Abstract
Potassium (K⁺) is an essential macronutrient for plant growth and development. Previous studies have demonstrated that Calcineurin B-Like Protein1 (CBL1) or CBL9 and CBL-Interacting Protein Kinase23 (CIPK23) regulate K⁺ uptake in Arabidopsis (Arabidopsis thaliana) roots by modulating K⁺ channel Arabidopsis K⁺ Transporter1. In this study, we show that the protein kinase CIPK9 interacts with the calcium sensor CBL3 and plays crucial roles in K⁺ homeostasis under low-K⁺ stress in Arabidopsis. Arabidopsis wild-type plants showed leaf chlorotic symptoms when grown for 10 d on low-K⁺ (100 μM) medium. Here, we show that plants lacking CIPK9 displayed a tolerant phenotype to low-K⁺ stress, which still maintained green leaves when the wild-type plants showed typical K⁺-deficient symptoms. Overexpressing lines of CIPK9 resulted in a low-K⁺-sensitive phenotype compared with wild-type plants. Furthermore, CBL2 and CBL3 were identified as upstream regulators of CIPK9. Both CBL2- and CBL3-overexpressing lines displayed similar low-K⁺-sensitive phenotypes and K⁺ contents to CIPK9-overexpressing lines. However, only cbl3 mutant plants, but not cbl2 mutant plants, showed the low-K⁺-tolerant phenotype similar to cipk9 mutants. Taken together, these results demonstrate that CIPK9 and CBL3 work together and function in K⁺ homeostasis under low-K⁺ stress in Arabidopsis.