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<p>Strawberry fruit softening, a&#xa0;major factor limiting shelf life, is closely associated with pectin disassembly in the cell wall. Calcium (Ca) treatment is a&#xa0;common strategy to improve fruit firmness, but its efficacy varies with Ca source and application protocol. This study systematically compared the effects of five different foliar Ca sources on fruit firmness, pectin metabolism, and the expression of related genes in strawberry (<i>Fragaria</i> × <i>ananassa</i> Duch. cv. ‘Jingmei&#xa0;1’). The impact of Ca treatments on fruit firmness was inconsistent and time-dependent. Notably, all Ca treatments, especially sugar–alcohol–Ca, significantly increased the contents of covalently bound pectin (CBP), ionically bound pectin (IBP), and water-soluble pectin (WSP) across three fruit developmental stages. Contrary to common assumptions, Ca treatments generally activated, rather than inhibited, the activities of key cell wall-degrading enzymes: pectin esterase (PE), β‑galactosidase (β-Gal), polygalacturonase (PG), and pectate lyase (PL). At the transcriptional level, Ca treatments differentially regulated the expression of corresponding genes (<i>FaPE1, Faβ-gal4, FaPG1, FaPL4</i>). The effect of Ca on strawberry fruit firmness is the net outcome of a&#xa0;dynamic balance between its physical cross-linking action, which stabilizes pectin, and its metabolic regulatory role, which promotes pectin accumulation and activates cell wall metabolism. To reliably enhance firmness, efficient Ca sources such as calcium nitrate or sugar–alcohol–Ca should be applied during the early fruit development window, avoiding excessively high concentrations of calcium chloride (CaCl<sub>2</sub>).</p>

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Effects of Foliar Calcium Application on Firmness, Pectin Dynamics, and Gene Regulation in Strawberry Fruit

  • 期刊论文

  • 发表日期：

    2026年5月11日

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  • Zihan Geng,
  • Qiushi Li,
  • Chunwen Yu,
  • Yu Wang,
  • Deguo Han,
  • Jing Dong

摘要

Strawberry fruit softening, a major factor limiting shelf life, is closely associated with pectin disassembly in the cell wall. Calcium (Ca) treatment is a common strategy to improve fruit firmness, but its efficacy varies with Ca source and application protocol. This study systematically compared the effects of five different foliar Ca sources on fruit firmness, pectin metabolism, and the expression of related genes in strawberry (Fragaria × ananassa Duch. cv. ‘Jingmei 1’). The impact of Ca treatments on fruit firmness was inconsistent and time-dependent. Notably, all Ca treatments, especially sugar–alcohol–Ca, significantly increased the contents of covalently bound pectin (CBP), ionically bound pectin (IBP), and water-soluble pectin (WSP) across three fruit developmental stages. Contrary to common assumptions, Ca treatments generally activated, rather than inhibited, the activities of key cell wall-degrading enzymes: pectin esterase (PE), β‑galactosidase (β-Gal), polygalacturonase (PG), and pectate lyase (PL). At the transcriptional level, Ca treatments differentially regulated the expression of corresponding genes (FaPE1, Faβ-gal4, FaPG1, FaPL4). The effect of Ca on strawberry fruit firmness is the net outcome of a dynamic balance between its physical cross-linking action, which stabilizes pectin, and its metabolic regulatory role, which promotes pectin accumulation and activates cell wall metabolism. To reliably enhance firmness, efficient Ca sources such as calcium nitrate or sugar–alcohol–Ca should be applied during the early fruit development window, avoiding excessively high concentrations of calcium chloride (CaCl2).