Fig. 6: abi1-1c and aba2-1 mutant plants are hypersensitive to external K⁺ deficiency.

a Representative images of wild type (Col-0), cipk9/23 double mutant, abi1-1c mutants under high- or low-K⁺ in post-germination assays. The seedlings were grown under sufficient-K⁺ (20 mM) conditions for 4 days, followed by a transfer to high-K⁺ (20 mM) or low-K⁺ (5 μM) condition and grown for another 5 days. b Measurement of root length at the end of the assay as shown in a. c Growth phenotype of 5-week-old plants of Col-0, cipk9/23 double mutant, abi1-1c and aba2-1 mutants in hydroponic solutions containing high- or low-K⁺. 7-day-old seedlings germinated on MS plates were transferred to hydroponic solutions containing high-K⁺ (20 mM) or low-K⁺ (10 μM) for another 4 weeks. Photographs were taken at the end of the assay. d Measurement of the fresh weight of plants in hydroponic solutions as shown in d. e Quantification of K content in various plant materials was measured at the end of the K⁺-starvation assay as shown in c. Data in b, d, and e are shown as mean ± SD, n = 3 (biologically independent experiments). Statistical analysis between groups were performed by one-way analysis of variance (ANOVA) followed by a Tukey’s multiple comparison test. f A working model depicting the regulation of dual CBL-CIPK modules in plant responses to changes in K⁺ status. Low-K⁺ stress enhances protein abundance and phosphorylation of Ca²⁺ sensors (vacuolar CBL2/3, plasma membrane CBL1/9) and their CIPK partners. The dual CBL-CIPK modules activate target transporters such as TPK1 and AKT1to increase K remobilization and uptake, which ultimately enable plants to adapt to low-K⁺ conditions. Upon K⁺-repletion, dual CBL-CIPK modules are deactivated through dephosphorylation and protein degradation. The PP2C family phosphatases, including HAB1/ABI1/ABI2/PP2CA, specifically deactivate the vacuolar CBL-CIPK module.