Fig. 4.

A systematic model illustrating the cross-talk between melatonin (MT) and nitric oxide (NO) in plant cells. During abiotic stresses, NO is produced and induces the tryptophan decarboxylase (TDC), and tryptamine (Trm) is further hydroxylated by tryptamine 5- hydroxylase (T5H) to serotonin. In a subsequent step, serotonin is converted to 5-methyltryptamine, and serotonin N-acetyltransferase (SNAT) acetylate 5-methyltryptamine to synthesize MT under stress conditions. The compound sodium nitroprusside (SNP), acts as a NO source and protects against abiotic stresses. The addition of SNP inhibited the synthesis of hydroxyindole-O-methyltransferase (HIOMT; a MT synthase; however, the expression of HIOMT was up-regulated in the presence of exogenous MT or abiotic stress. The exogenous MT also up-regulates ZATs, which bind with CBFs and trigger the synthesis of l-arginine from the arginine pathway. NOS converts l-arginine to NO, further converted into S-nitrosoglutathione (GSNO) by reduced glutathione (GSH). GSNO subsequently breakdown into NO and releases S-nitrosylation (SNO) by the action of S-nitrosoglutathione reductase. In response to stress, Nitrate reductase (NR) also activate to produce NO. The combined effect of MT and NO regulates the MAPK cascade, further activating the metal-responsive transcription factor-1 (MTF-1) and alleviating heavy metal toxicity in plants. On the other hand, SNO promotes histone deacetylase (HDA19) to inhibit the acetylation of histone, leading to CBF gene suppression.