Abstract
Chitosan (CTS) plays an important role in delaying fruit ripening and extending fruit shelf life when used as an eco-friendly and edible coating. However, there is still limited understanding about the molecular mechanisms and effects of chitosan on the quality of postharvest kiwifruit. In this study, firmness, total soluble solid, acid, phenolic content, flavonoid content, starch and ascorbic acid concentration, ethylene production, and cell-wall components were determined after CTS treatment. Fruit treated with CTS maintained higher firmness, starch and flavonoids (3.85-, 1.78-and 2.08-fold higher, respectively, after 6d compared to the control). Widely targeted metabolome analysis revealed flavonoids (dihydrokaempferol-7-O-glucoside, eriodictyol-3′-O-glucoside) and lipids (LysoPC 16:0 (2 n isomer)), and punicic acid (9Z,11E,13Z-octadecatrienoic acid) were the main differential metabolites. KEGG pathway enrichment analysis showed ‘metabolic pathways (ko01100)’ and ‘biosynthesis of secondary metabolites (ko01110)’ were the main KEGG pathways. Integrated metabolomic and transcriptomic analyses revealed that the expression of five key structural genes, including three starch degradation genes (AcBAM3L, AcBAM3.1, Acc31818 (PHS)), one cell-wall modification gene (AcPG1), and one flavonoids biosynthesis gene (Acc18331 (F3'H)), and 12 transcription factors (AcNAC083, AcRAP2–10, AcERF14, AcERF64, Acc27131 (bZIP), AcHSFB2a, Acc12589 (IAA), AcMYB13, Acc20159 (bHLH), AcBEL1, AcbHLH149, AcWRKY75) were different. Real-time PCR analyses verified that the expression of AcBAM3L, AcBAM3.1, AcPG1 and most of the 12 transcription factors were suppressed by CTS treatment, while the expression of Acc31818 (PHS), Acc18331 (F3'H) and AcBEL1 were enhanced by CTS treatment. Together, these CTS-responsive genes may play critical roles in determining the rate of ripening and quality change of postharvest kiwifruit.
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