Transcriptome, degradome and physiological analysis provide new insights into the mechanism of inhibition of litchi fruit senescence by melatonin.

Litchi fruit has high commercial value on the international market, but senesces rapidly after harvest. We used weighted gene co-expression network analysis (WGCNA) and degradome technology to investigate the molecular mechanisms of melatonin-mediated delay of litchi fruit senescence through application of exogenous melatonin and p-chlorophenylalanine (p-CPA, an inhibitor of melatonin biosynthesis) treatments. Results demonstrated that exogenous melatonin treatment delayed litchi fruit senescence while p-CPA accelerated senescence. Coupled analyses of transcriptome and physiological parameters of litchi fruit provided the correlation of network modules with dynamic changes in browning index during storage. Additionally, we found that microRNAs (miR858 and miR160a) and their targets were actively involved in melatonin-mediated delay of litchi fruit senescence. Melatonin treatment decreased abscisic acid (ABA) content but increased PP2C and F-box expression levels, suggesting the involvement of ABA signaling in melatonin-mediated antisenescence. The transcriptions of ZAT, NAC and DREB1 were activated by melatonin treatment. Moreover, the major functional genes involved in histone methylation, γ-aminobutyric acid (GABA) metabolism, energy production, reactive oxygen species (ROS) accumulation and cell death were identified in the melatonin-inhibited litchi pericarp browning. Taken together, we first constructed the global map of the important regulators and pathways to delay litchi senescence and pericarp browning mediated by melatonin.