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Rice is a staple food for over half of the global population, and the postharvest quality deterioration of paddy rice is closely linked to lipid degradation. Low-temperature storage represents an effective strategy for maintaining rice quality and achieving green storage. However, the intrinsic mechanisms by which prolonged low-temperature storage coordinately regulates rice lipid metabolism at the level of metabolite dynamics and gene expression networks to maintain its stability have not been fully elucidated.
This study aimed to integrate multi-omics technologies to systematically elucidate biochemical and molecular mechanisms underlying lipid stability in japonica rice during long-term low-temperature storage.
Fresh Nanjing 46 paddy rice was stored at 25 and 15 ℃ for 360 days, with sampling every 30 days. An integrated approach combining physiological and biochemical analyses, lipidomics, and transcriptomics was employed to systematically investigate stabilization mechanisms.
Low-temperature storage effectively maintained rice lipid stability through a multi-layered regulatory network. Regarding membrane lipid metabolism, low-temperature storage downregulated PLDα1, thereby delaying the hydrolysis of phospholipids, including phosphatidylethanolamine, phosphatidylinositol, and phosphatidylcholine, and helping to maintain cellular membrane integrity. Additionally, reduced expression of OsCDase limited sphingolipid degradation, further enhancing plasma membrane stability. In terms of lipid hydrolysis, lipase activity was suppressed under low-temperature conditions, inhibiting triglyceride hydrolysis. In oxidative metabolic pathways, the downregulation of OsFAD2 and ACX1 genes inhibited polyunsaturated fatty acid synthesis and β-oxidation, thus alleviating oxidative stress. Reduced lipoxygenase (LOX,Lipoxygenase) activity at low temperatures further mitigated the oxidation of unsaturated fatty acids, thereby minimizing off-flavor formation.
During rice storage, lipid hydrolysis served as a critical precursor to oxidation, with both processes jointly determining quality deterioration. Low-temperature storage simultaneously inhibited lipid hydrolysis and oxidation pathways, consequently maintaining lipid compositional stability at the metabolomic level and delaying quality decline at the phenotypic level.
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