Melatonin Enhances Drought Tolerance by Regulating Leaf Stomatal Behavior, Carbon and Nitrogen Metabolism, and Related Gene Expression in Maize Plants

It is commonly known that exogenously applied melatonin can alleviate the impact of drought stress, but the mechanism used by melatonin to regulate stomatal behavior and carbon (C) and nitrogen (N) metabolism to increase drought resistance remains elusive. Herein, our aim was to investigate the influence of exogenous melatonin on the regulation of C and N metabolism in maize plants under water deficit. In this study, we analyzed stomatal behavior, the key components of C and N metabolism, and the gene expression and activity of enzymes involved in the C and N metabolism in maize plants. The results showed that the application of melatonin (100 μM) significantly increased maize growth and sustained the opening of stomata, and secondarily increased the photosynthetic capacity in maize. Under drought stress, foliar application of melatonin induced the gene transcription and activities of sucrose phosphate synthetase, ADP-glucose pyrophosphorylase, phosphoenolpyruvate carboxylase, and citrate synthase, resulting in the enhancement of sucrose and starch synthesis and the tricarboxylic acid (TCA) cycle. This enhancement in sugar biosynthesis and the TCA cycle might lead to stronger N assimilation. As anticipated, NO(3)(–) reduction and NH(4)(+) assimilation were also strengthened after melatonin treatment under drought stress. An increase was observed in some key enzymatic activities and transcription involved in nitrogen metabolism, such as that of nitrate reductase, nitrite reductase, glutamate synthase, and glutamine synthetase, in melatonin-treated, drought-stressed maize. Moreover, melatonin attenuated the drought-induced damage by reducing protein degradation and increasing the level of proline. Conclusively, our results indicate that exogenous melatonin enhances drought tolerance in maize via promoting stomatal opening and regulating C and N metabolism and related gene expression.