Melatonin is a multifunctional signaling molecule that regulates broad aspects of responses to environmental stresses in plants. Cadmium (Cd) is a persistent soil contaminant that is toxic to all living organisms. Recent reports have uncovered the protective role of melatonin in alleviating Cd phytotoxicity, but little is known about its regulatory mechanisms in plants. In this study, we found that foliar application of melatonin (in particular 100 μmol L-1) remarkably enhanced Cd tolerance of tobacco (Nicotiana tabacum L.) leaves, as evidenced by less Cd accumulation and alleviation of growth inhibition and photoinhibition, compared with nontreated Cd-stressed plants. The addition of melatonin also controlled oxidative damage of Cd on tobacco through direct scavenging and by enhancing the activities of antioxidative enzymes. Melatonin application promoted Cd sequestration in the cell wall and vacuoles based on the analysis of subcellular distribution of Cd in tobacco cells. Structural equation modeling (SEM) analysis revealed that melatonin-induced Cd tolerance in tobacco leaves was modulated by the expression of Cd-transport genes. Molecular evidence illustrated that modulation of IRT1, Nramp1, HMA2, HMA4, and HMA3 genes caused by melatonin could be responsible for weakening Cd uptake, Cd transportation to xylem, and intensifying Cd sequestration into the root vacuoles.
Keywords: Antioxidation; Cadmium tolerance; Melatonin; Molecular regulation; Tobacco.
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