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Voltage-gated K + channel β subunits act as a structural component of K in channels in different species. The β subunits are not essential to the channel activity but confer different properties through binding the T1 domain or the C-terminal of α subunits. Here, we studied the physiological function of a novel gene, KIbB1 , encoding a voltage-gated K + channel β subunit in sweetpotato. The transcriptional level of this gene was significantly higher in the low-K + -tolerant line than that in the low-K + -sensitive line under K + deficiency conditions. In Arabidopsis , KIbB1 positively regulated low-K + tolerance through regulating K + uptake and translocation. Under high-salinity stress, the growth conditions of transgenic lines were obviously better than wild typr (WT). Enzymatic and non-enzymatic reactive oxygen species (ROS) scavenging were activated in transgenic plants. Accordingly, the malondialdehyde (MDA) content and the accumulation of ROS such as H 2 O 2 and O 2- were lower in transgenic lines under salt stress. It was also found that the overexpression of KIbB1 enhanced K + uptake, but the translocation from root to shoot was not affected under salt stress. This demonstrates that KIbB1 acted as a positive regulator in high-salinity stress resistance through regulating Na + and K + uptake to maintain K + /Na + homeostasis. These results collectively suggest that the mechanisms of KIbB1 in regulating K + were somewhat different between low-K + and high-salinity conditions.

The Sweetpotato Voltage-Gated K+ Channel β Subunit, KIbB1, Positively Regulates Low-K+ and High-Salinity Tolerance by Maintaining Ion Homeostasis