The Ca(2+)-CaM Signaling Pathway Mediates Potassium Uptake by Regulating Reactive Oxygen Species Homeostasis in Tobacco Roots Under Low-K(+) Stress

Potassium (K(+)) deficiency severely threatens crop growth and productivity. Calcium (Ca(2+)) signaling and its sensors play a central role in the response to low-K(+) stress. Calmodulin (CaM) is an important Ca(2+) sensor. However, the mechanism by which Ca(2+) signaling and CaM mediate the response of roots to low-K(+) stress remains unclear. In this study, we found that the K(+) concentration significantly decreased in both shoots and roots treated with Ca(2+) channel blockers, a Ca(2+) chelator, and CaM antagonists. Under low-K(+) stress, reactive oxygen species (ROS) accumulated, and the activity of antioxidant enzymes, NAD kinase (NADK), and NADP phosphatase (NADPase) decreased. This indicates that antioxidant enzymes, NADK, and NADPase might be downstream target proteins in the Ca(2+)-CaM signaling pathway, which facilitates K(+) uptake in plant roots by mediating ROS homeostasis under low-K(+) stress. Moreover, the expression of NtCNGC3, NtCNGC10, K(+) channel genes, and transporter genes was significantly downregulated in blocker-treated, chelator-treated, and antagonist-treated plant roots in the low K(+) treatment, suggesting that the Ca(2+)-CaM signaling pathway may mediate K(+) uptake by regulating the expression of these genes. Overall, this study shows that the Ca(2+)-CaM signaling pathway promotes K(+) absorption by regulating ROS homeostasis and the expression of K(+) uptake-related genes in plant roots under low-K(+) stress.