Crosstalk between melatonin and Ca2+/CaM evokes systemic salt tolerance in Dracocephalum kotschyi.

In this study, the role of calcium/calmodulin (Ca2+/CaM) and melatonin (Mel) as two signal molecules in inducing systemic salt tolerance of Dracocephalum kotschyi Boiss. was investigated. Salinity stress (100 mM NaCl) reduced plant growth and induced ionic, osmotic, and oxidative damages in D. kotschyi leaves. Detection of cytosolic free Ca2+ ([Ca2+]cyt) by the Fura-2 method and the measurement of endogenous Mel by GC-MS demonstrated that salinity induced Ca2+ burst and increased endogenous Mel content in D. kotschyi leaves. Root pretreatment with 5 mM Ca2+ or 100 μM Mel recovered plant growth, reduced leaf electrolytic leakage, H2O2, and MDA contents and improved membrane integrity not only at the application site (roots), but also at the untreated distal parts (leaves) under salt stress. Rhizospheric treatment with Mel and Ca2+ triggered systemic tolerance in D. kotschyi, as judged from improving RWC, increasing proline content, modulating Na+, K+, and Ca2+ homeostasis, and enhancing the activities of SOD, CAT, APX, and POD in the leaves of salt-stressed plants. Mel augmented [Ca2+]cyt, but the rhizospheric application of Ca2+ antagonists impaired the latter responses. Furthermore, root pretreatment with Ca2+ increased Mel content, but the application of p-chlorophenylalanine (as an inhibitor of Mel biosynthesis) decreased the above attributes in the leaves of Ca2+-treated plants, leading to an arrest in the Ca2+-induced systemic salt tolerance. These novel results suggest that interaction of Ca2+/CaM and Mel is involved in overcoming salt-induced ionic, osmotic, and oxidative damages and Ca2+ and Mel may act as long-distance signals for inducing systemic salt tolerance in D. kotschyi.