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    In: Journal of the Science of Food and Agriculture, Wiley, Vol. 103, No. 12 ( 2023-09), p. 6055-6069
    Kurzfassung: Actinidia eriantha is one of the most important kiwifruit species in Actinidia . The relative high accumulation of organic acids in fruit of A. eriantha is an unfavorable factor for organoleptic quality. To identify key metabolic enzymes and genes involved in organic acids accumulation during fruit development, physiological, biochemical, and molecular experiments were conducted for the dynamic fruit samples of a new kiwifruit cultivar, A. eriantha ‘Ganlv 1’. RESULTS The contents of citric acid and malic acid increased greatly during fruit development, while quinic acid content decreased obviously. Significant positive correlations were observed between fruit titratable acidity and the contents of both citric acid and malic acid, and a significant negative correlation was found between fruit titratable acidity and the quinic acid content. The high accumulation of citric acid was found to be caused by the increased activity of citrate synthase (CS), and the decreased activities of two degradation‐related enzymes, mitochondrial aconitase and nicotinamide adenine dinucleotide (NAD)‐dependent isocitrate dehydrogenase. In addition, the accumulation of malic acid depended mainly on the increased synthesis catalyzed by NAD‐dependent malate dehydrogenase (NAD‐MDH) and phosphoenolpyruvate carboxylase. Further analysis suggested that AeCS2 and AeMDH2 played pivotal roles in controlling the activities of CS and NAD‐MDH respectively. CONCLUSION The high accumulation level of citric acid relied on both the strong synthesis ability and the weak degradation ability. The accumulation level of malic acid was mainly affected by the synthesis. The novel information would be helpful for our understanding of the formation of fruit acidity quality. © 2023 Society of Chemical Industry.
    Materialart: Online-Ressource
    ISSN: 0022-5142 , 1097-0010
    URL: Issue
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2023
    ZDB Id: 2001807-1
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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