| Summary: | Voltage-gated K<sup>+</sup> channel β subunits act as a structural component of K<sub>in</sub> 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, <i>KIbB1</i>, encoding a voltage-gated K<sup>+</sup> channel β subunit in sweetpotato. The transcriptional level of this gene was significantly higher in the low-K<sup>+</sup>-tolerant line than that in the low-K<sup>+</sup>-sensitive line under K<sup>+</sup> deficiency conditions. In <i>Arabidopsis</i>, <i>KIbB1</i> positively regulated low-K<sup>+</sup> tolerance through regulating K<sup>+</sup> 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<sub>2</sub>O<sub>2</sub> and O<sup>2−</sup> were lower in transgenic lines under salt stress. It was also found that the overexpression of <i>KIbB1</i> enhanced K<sup>+</sup> uptake, but the translocation from root to shoot was not affected under salt stress. This demonstrates that <i>KIbB1</i> acted as a positive regulator in high-salinity stress resistance through regulating Na<sup>+</sup> and K<sup>+</sup> uptake to maintain K<sup>+</sup>/Na<sup>+</sup> homeostasis. These results collectively suggest that the mechanisms of <i>KIbB1</i> in regulating K<sup>+</sup> were somewhat different between low-K<sup>+</sup> and high-salinity conditions.
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