Abstract
Flowering Chinese cabbage is prone to withering, yellowing and deterioration after harvest. Melatonin plays a remarkable role in delaying leaf senescence and increasing flavonoid biosynthesis. However, the underlying molecular mechanisms of melatonin procrastinating postharvest senescence by regulating flavonoid biosynthesis remain largely unknown. In this study, melatonin could promote flavonoid accumulation and delay the postharvest senescence of flowering Chinese cabbage. Surprisingly, we observed that BrFLS1 and BrFLS3.2 were core contributors in flavonoid biosynthesis, and BrERF2 and BrERF109 were crucial ethylene response factors (ERFs) through the virus-induced gene silencing (VIGS) technique, which is involved in regulating the postharvest senescence under melatonin treatment. Furthermore, yeast one-hybrid (Y1H), dual luciferase (LUC), and β-glucuronidase (GUS) tissue staining experiments demonstrated that BrERF2/BrERF109 negatively regulated the transcripts of BrFLS1 and BrFLS3.2 by directly binding to their promoters, respectively. Silencing BrERF2/BrERF109 significantly upregulated the transcripts of BrFLS1 and BrFLS3.2, promoting flavonoid accumulation, and postponing the leaf senescence. Our results provided a new insight into the molecular regulatory network of melatonin delaying leaf senescence and initially ascertained that melatonin promoted flavonoid accumulation by suppressing the inhibition of BrERF2/BrERF109 on the transcripts of BrFLS1 and BrFLS3.2, which led to delaying the leaf senescence of postharvest flowering Chinese cabbage.