Abstract

Melatonin treatment delayed endocarp browning of postharvest longan fruit. • Melatonin application suppressed the accumulations of H₂O₂ and MDA of longan pericarp. • Melatonin treatment activated the antioxidant system of longan pericarp. • NAC083 was significantly induced by exogenous melatonin at the early storage stage. • NAC083 bound to the promoter region of RbohD-3 and repressed its transcription. Longan ( Dimocarpus longan ) as an important subtropical fruit exhibit a high nutritional and commercial value. Postharvest longan fruit undergo a rapid senescence, as characterized with endocarp browning. In this study, melatonin was applied to longan fruit to examine the mediated-browning during storage at 25 °C. Application of 0.1 mM melatonin significantly delayed endocarp browning, reduced respiration rate and the contents of H₂O₂ and malondialdehyde (MDA), and increased the activities of superoxide dismutase (SOD) and peroxidase (POD) at the early stage and catalase (CAT) activity throughout the storage period in longan fruit. Furthermore, two NAC famliy transcription factors, NAC083 and ATAF1, were used to investigate the endocarp browning of longan fruit during storage. The expression levels of both NAC083 and ATAF1 were upregulated in longan pericarp. Exogenous melatonin induced significantly the NAC083 expression in the pericarp at the early storage stage. Furthermore, DNA affinity purification and sequencing (DAP-seq), electrophoretic mobility shift assay (EMSA), dual-luciferase reporter (DLR), and stable transformation of longan root assay collectively confirmed that NAC083 can bind to the promoter region of respiratory burst oxidase homolog D-3 ( RbohD-3 ), a key gene in ROS metabolic pathway, and then inhibit its transcription. This study provides new insights into the involvement of the NAC083- RbohD-3 module in the reactive oxygen species (ROS)-mediated endocarp browning of longan fruit during storage.