The effect of 1-methylcyclopropene, methyl jasmonate and methyl salicylate on lignin accumulation and gene expression in postharvest ‘Xuxiang’ kiwifruit during cold storage

• Lignin gradually accumulated from the stem end to the calyx end in kiwifruit.
• Partial sequences of four lignin-associated genes were isolated.
• Methyl jasmonate and methyl salicylate application decreased lignin content.
• Lignin accumulation was boosted by 1-methylcyclopropene via AcPOD1 upregulation.

Kiwifruit is susceptible to chilling injury during storage at 0 °C, which causes lignin accumulation, a substantial impact to fruit quality. Lignin has been observed in the pulp and core of kiwifruit (Actinidia deliciosa cv. Xuxiang), developing gradually from the stem end to the calyx end. Fruit firmness can be maintained at a higher level during cold storage through application of 1-methylcyclopropene (1-MCP), although with dramatically enhanced activities of phenylalanine ammonia-lyase (PAL, EC 4.3.1.5), cinnamyl-alcohol dehydrogenase (CAD, EC 1.1.1.195), and peroxidase (POD, EC 1.11.1.7) as well as lignification, which occurred during the later storage period. Methyl jasmonate (MeJA) and methyl salicylate (MeSA) significantly inhibited lignification at later stages. Expression profiles of the four lignin-related genes (i.e., AcPAL, AcCAD, AcPOD1, and AcPOD2) were assessed, 1-MCP markedly increased the expression levels of AcPOD1 in fruit core tissue. Together, these results illustrate that MeJA and MeSA can inhibit lignin accumulation to some degree; however, 1-MCP may aggravate lignin deposition, especially in core tissue, mainly via up-regulating AcPOD1, which is involved in lignin synthesis.