Potassium (K) is an essential inorganic nutrient needed by plants for their growth and development. The conserved target of rapamycin (TOR) kinase, a well-known nutrition signaling integrator, has crucial roles in regulating growth and development in all eukaryotes. Emerging evidence suggests that TOR is a core regulator of nutrient absorption and utilization in plants. However, it is still unclear whether there is a causative link between the TOR pathway and potassium absorption. Here, we show that the expression of some potassium transporters and channels was regulated by TOR, and the suppression of TOR activity significantly affected potassium uptake in Arabidopsis and potato. Furthermore, we discovered that a Type 2A phosphatase-associated protein of 46 kDa (TAP46), a direct TOR downstream effector, could interact with CBL-interacting protein kinase 23 (CIPK23) in Arabidopsis and potato. In Arabidopsis, the K+ channel AKT1 conducting K+ uptake was significantly regulated by Calcineurin B-like Calcium Sensor Protein 1/9 (CBL1/9)-CIPK23 modules. We found that the cbl1cbl9, cipk23 (lks1-2 and lks1-3), and akt1 mutants were more hyposensitive to the TOR inhibitor than the wild-type, and the TOR inhibitor induced the downregulation of K+ uptake rate in the wild-type more than in these mutants. In addition, the overexpression of CIPK23 could effectively restore the defects in growth and potassium uptake induced by the TOR inhibitors. Thus, our work reveals a link between TOR signaling and CIPK23 and provides new insight into the regulation of potassium uptake in plants.
Keywords: CIPK23; Potassium channels; Potassium uptake; Potato; TAP46-PP2A; Target of rapamycin.
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