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Melatonin is an important bioactive molecule in plants. Two synthetases, N-acetylserotonin methyltransferase (ASMT) and serotonin N-acetyltransferase (SNAT) are involved in the final two steps of melatonin synthesis. Melatonin participates in responses to a variety of biotic and abiotic stresses in plants, but few studies have addressed the roles of endogenous melatonin in pathogen resistance. We investigated the role of endogenous melatonin in resistance to  Botrytis cinerea  infection in an  Arabidopsis thaliana  model system. Plant lines that overexpressed  ASMT  or  SNAT  through genetic manipulation showed upregulated expression of resistance genes  PR1  and  PR5 , transcription factor gene  WRKY33 , and jasmonic acid (JA) defense pathway marker gene  PDF1.2 , and downregulated transcription factor gene  MYC2  in JA signaling pathway. Higher melatonin content also enhanced the activity of antioxidant enzymes superoxide dismutase (SOD) and peroxidase (POD), increased JA content, reduced plant disease symptoms, and reduced lesion size in leaves. These findings indicate that endogenous melatonin enhances plant resistance to  B. cinerea  infection. In contrast,  ASMT  and  SNAT  gene silencing lines showed opposite results and were more susceptible to  B. cinerea . Thus, it can be demonstrated that melatonin functions as an effective regulator of plant stress resistance at the genetic level. A schematic model is presented for its role in resistance to  B. cinerea  infection. Our findings also helped to elucidate the associated signal transduction pathways and interactions between melatonin and other plant hormones.

Roles of Endogenous Melatonin in Resistance to Botrytis cinerea Infection in an Arabidopsis Model