Fig. 3.

A regulatory model of interaction between melatonin (MT) and secondary messengers under abiotic stress. During cold stress, the membrane-bounded phospholipid phosphatidylcholine (PC) is degraded by phospholipase D (PLD) to produce phosphatidic acid (PA), which subsequently modulates the protein phosphatase 2A (PP2A), nitrate reductase (NR), nitric oxide (NO), and H₂S. The exogenous application of MT triggers the Ca²⁺ channel to release Ca²⁺, which binds directly to the N-terminus of respiratory burst oxidase homologs (RBOHs), cold-induced Ca²⁺ activates respiratory burst oxidase activity to produce H₂O₂, thereby provoking Ca²⁺ transients in plant cells and causing downstream responses involving CBF-dependent pathways that promote cold tolerance. In case of salt stress, the PA is phosphorylated into cytidine diphosphate-diacylglycerol (CDP-DG), phosphatidylinositol (PtdIns), phosphatidylinositol bisphosphate (Ptd InsP2). The addition of MT up-regulates the phospholipase C (PLC), which hydrolysis the Ptd InsP2 into inositol 1,4,5 triphosphate (InsP3) and phosphorylated in subsequent steps to form phytic acid (InsP6), which triggers the release of Ca²⁺ in the cytoplasm. The MT receptor CAND2/PMTR1 also involves in the accumulation of Ca²⁺ by triggering G-protein G $\alpha$, which promotes ROS and Ca²⁺ production. Increased MT and Ca²⁺ influx up-regulates the transcription factors (AP2, bHLH, WRKY) to mitigate salt stress.