<p>Methyl jasmonate (MeJA) has been widely shown to mitigate chilling injury (CI) but the underlying mechanisms in peach remain largely unknown. Further, most MeJA studies focus on white-fleshed, rather than the more CI-resistant, yellow-fleshed peaches. To address this knowledge gap, we integrated lipidomic, volatile organic compound (VOC), and transcriptomic analyses to elucidate the mechanisms underlying MeJA protection in yellow-fleshed peaches. We identified ethyl acetate and methyl cinnamate as potential early biomarkers of CI right after cold storage. Our lipidomic characterization revealed that after 21&#xa0;days of cold storage at 5&#xa0;°C, MeJA-treated peaches showed increased phospholipid levels and reduced triacylglycerols and diacylglycerols compared to control fruit. Additionally, membrane lipids in MeJA-treated peaches exhibited greater unsaturation in fatty acids, particularly an increase in linolenic acid, which may contribute to membrane integrity and aroma enhancement. VOC analysis supported this, revealing significant alterations in 11 out of 20 compounds, including higher levels of γ-decalactone and δ-decalactone, key contributors to peach flavor, in MeJA-treated peaches. Interestingly, transcriptomic analysis showed limited differential expression in lipid- and VOC-related genes, despite the considerable differences observed. Instead, Gene Ontology enrichment analysis indicated upregulation of autophagy-related genes in response to MeJA treatment. Together, our findings suggest that MeJA alleviates CI in yellow-fleshed peach via modulation of lipid composition and metabolism, with autophagy potentially contributing as an additional regulatory process.</p>

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Postharvest methyl jasmonate dipping modulates lipid composition and volatile profiles to alleviate chilling injury in yellow-fleshed peach fruit

  • Po-Kai Huang,
  • Diane M. Beckles,
  • Pedro J. Martínez-García,
  • Carlos H. Crisosto

摘要

Methyl jasmonate (MeJA) has been widely shown to mitigate chilling injury (CI) but the underlying mechanisms in peach remain largely unknown. Further, most MeJA studies focus on white-fleshed, rather than the more CI-resistant, yellow-fleshed peaches. To address this knowledge gap, we integrated lipidomic, volatile organic compound (VOC), and transcriptomic analyses to elucidate the mechanisms underlying MeJA protection in yellow-fleshed peaches. We identified ethyl acetate and methyl cinnamate as potential early biomarkers of CI right after cold storage. Our lipidomic characterization revealed that after 21 days of cold storage at 5 °C, MeJA-treated peaches showed increased phospholipid levels and reduced triacylglycerols and diacylglycerols compared to control fruit. Additionally, membrane lipids in MeJA-treated peaches exhibited greater unsaturation in fatty acids, particularly an increase in linolenic acid, which may contribute to membrane integrity and aroma enhancement. VOC analysis supported this, revealing significant alterations in 11 out of 20 compounds, including higher levels of γ-decalactone and δ-decalactone, key contributors to peach flavor, in MeJA-treated peaches. Interestingly, transcriptomic analysis showed limited differential expression in lipid- and VOC-related genes, despite the considerable differences observed. Instead, Gene Ontology enrichment analysis indicated upregulation of autophagy-related genes in response to MeJA treatment. Together, our findings suggest that MeJA alleviates CI in yellow-fleshed peach via modulation of lipid composition and metabolism, with autophagy potentially contributing as an additional regulatory process.