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

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.