Potassium is an essential mineral element for plant growth and development. Although it is known that plants absorb and transport K+ through membrane transporters, it remains unclear how these transporters are regulated. Here we show that the protein kinase CIPK23, encoded by the LKS1 gene, regulates K+ uptake under low-K+ conditions. Lesion of LKS1 significantly reduced K+ uptake and caused leaf chlorosis and growth inhibition, whereas overexpression of LKS1 significantly enhanced K+ uptake and tolerance to low K+. We demonstrate that CIPK23 directly phosphorylates the K+ transporter AKT1 and further find that CIPK23 is activated by the binding of two calcineurin B-like proteins, CBL1 and CBL9. We propose a model in which the CBL1/9-CIPK23 pathway ensures activation of AKT1 and enhanced K+ uptake under low-K+ conditions.

As one of the most important mineral nutrient elements, potassium (K(+)) participates in many plant physiological processes and determines the yield and quality of crop production. In this review, we summarize K(+) signaling processes and K(+) transport regulation in higher plants, especially in plant responses to K(+)-deficiency stress. Plants perceive external K(+) fluctuations and generate the initial K(+) signal in root cells. This signal is transduced into the cytoplasm and encoded as Ca(2+) and reactive oxygen species signaling. K(+)-deficiency-induced signals are subsequently decoded by cytoplasmic sensors, which regulate the downstream transcriptional and posttranslational responses. Eventually, plants produce a series of adaptive events in both physiological and morphological alterations that help them survive K(+) deficiency.

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