Exogenous calcium reduces postharvest loss of muskmelon fruit by promoting suberin polyaliphatic deposition

Ca²⁺ acts as a pivotal second messenger in plants, activating downstream signaling components that enhance resistance to both abiotic and biotic stresses. Suberin polyaliphatic (SPA) is a major component of the protective barriers in wounded fruit. However, it is unknown whether exogenous calcium treatment can reduce postharvest losses by promoting SPA deposition. This study investigated how calcium treatment promotes the accumulation of SPA in postharvest muskmelon.

Treatment with 1 mm CaCl₂ enhanced the activity and gene expression of succinate dehydrogenase and malate dehydrogenase, raising ATP and energy charge, and providing energy for fatty acid synthesis. It also increased peroxidase and superoxide dismutase activity and gene expression, at the same time as upregulating calcium-dependent protein kinase (CmCDPK) and NADPH oxidase (CmNOX). This resulted in elevated O₂•^- and H₂O₂, serving as an oxidant for the cross-linking of suberin. Furthermore, calcium upregulated genes for fatty acid synthesis, boosting production of primary alcohols, α,ω-dicarboxylic acids, ω-hydroxy acids, fatty acids and glycerides. These responses accelerated SPA accumulation at wound sites, improving tissue texture, as well as reducing weight loss and disease index. By contrast, ethylene glycol tetraacetic acid, a specific Ca²⁺ chelator, sequestered endogenous Ca²⁺ in the wound tissues, thereby blocking calcium signaling and exerting inhibitory effects diametrically opposite to those of CaCl₂ treatment on healing processes, including energy metabolism, reactive oxygen species metabolism and SPA synthesis.

Collectively, CaCl₂ treatment accelerates fruit wound healing by increasing the accumulation of SPA at the wound site, thereby maintaining the quality of the fruit. EGTA treatment delayed wound healing by chelating Ca²⁺. © 2026 Society of Chemical Industry.