Melatonin induces improved protection against Botrytis cinerea in cherry tomato fruit by activating salicylic acid signaling pathway

Melatonin modulated immune responses to various stresses in plants. However, the crosstalk between melatonin and the other signal molecules, especially with salicylic acid (SA), is largely unclear in fruit. The objective of this research was to investigate the mechanism of melatonin induced disease resistance in cherry tomato fruit. The results indicated that melatonin treatment significantly inhibited gray mold development, induced reactive oxygen species (ROS) burst, enhanced SA accumulation accompanied by increasing its synthesis-related enzymes activity, up-regulated expression of defense genes, including SlWRKY70, SlNPR1, SlTGA5, SlPR1, SlPR2 and SlGLU, but decreased nitric oxide (NO) content during storage. Moreover, melatonin treatment increased endogenous melatonin content by up-regulating the expressions of SlTDC, SlSNAT and SlASMT in fruit during storage. However, the melatonin-enhanced disease resistance in fruit was completely abolished by a paclobutrazol (PAC) (SA biosynthesis inhibitor) treatment. Thus, the results suggested that hydrogen peroxide (H2O2) and SA signaling pathway would be collectively involved in melatonin induced-disease resistance in cherry tomato fruit during storage.

Automated summary

Melatonin treatment in cherry tomato fruit enhances disease resistance by inhibiting gray mold development, increasing SA accumulation and reactive oxygen species burst, up-regulating defense gene expression, and increasing endogenous melatonin content. However, the involvement of salicylic acid is necessary for melatonin-induced disease resistance.