6 research outputs found

    DataSheet_1_Comparative transcriptomic and metabolomic analyses reveal the delaying effect of naringin on postharvest decay in citrus fruit.zip

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    IntroductionNaringin exhibits antioxidant capacity and can partially inhibit pathogens in many horticultural products, such as citrus fruit; however, the effects of naringin on the storage quality and mechanisms that regulate senescence in citrus fruit have not been comprehensively analyzed.Methods and resultsIn this study, exogenous naringin treatment was found to significantly delay citrus fruit disease, decreasing the H2O2 content, increasing the antioxidant capacity and maintaining the quality of the fruit. Metabolomic analysis of citrus peel indicated the vast majority (325) of metabolites belonging to flavonoids. Moreover, the auraptene, butin, naringenin, and luteolin derivative levels within the phenylpropanoid pathway were significantly higher in the naringin-treated fruit than in the control fruit. Transcriptomic analysis also revealed that twelve genes in the phenylpropanoid and flavonoid biosynthesis pathways were significantly upregulated. Further analysis with a co-expression network revealed significant correlation between these differential genes and metabolites. Additionally, MYC and WRKY, screened from the MAPK signaling pathway, may contribute to naringin-induced disease resistance.ConclusionIn conclusion, naringin treatment can efficiently delay decay and maintain the quality of citrus fruit, mainly by promoting metabolites accumulation, and upregulating differentially expressed genes in phenylpropanoid and flavonoid biosynthesis pathway. This study provides a better understanding of the regulatory mechanisms through which naringin delays citrus fruit decay and maintains fruit quality.</p

    MOESM1 of Regioselectivity of oxidation by a polysaccharide monooxygenase from Chaetomium thermophilum

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    Additional file 1: Figure S1. SDS-PAGE of the purified Cu2+-CtPMO1 produced in Pichia pastoris. Figure S2. The N-terminal amino acid sequence analysis of CtPMO1 using LC-MS/MS. Figure S3. MALDI-TOF-MS/MS analysis of m/z 525 from MALDI-TOF-MS analysis. Figure S4. Types of fragmentation of CtPMO1 C4- and C6-oxidized products (m/z 525). Figure S5. 1H NMR spetra of CtPMO1 soluble reaction products with PASC as substrate in DMSO-d 6 . Figure S6. Sequence alignment of CtPMO1 and NCLPMO9C using ClastalW2. Figure S7. Homology model of the catalytic domain of CtPMO1 using SWISS-MODEL. Figure S8. Homology model of CtPMO1 binding with cellopentaose. Figure S9. Identification of the mutated CtPMO1 soluble reaction products oxidized by Br2 using with PASC as substrate MALDI-TOF-MS. Table S1. List of primers used for PCR of the CtPMO1 protein. Table S2. Fragmentation analysis of the peak of DP3-2 (m/z 525) according to Additional file 1: Figure S3, S4

    Table_1_Exogenous melatonin treatment affects ascorbic acid metabolism in postharvest ‘Jinyan’ kiwifruit.DOCX

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    Ascorbic acid (AsA) is an important nutritious substance in fruits, and it also can maintain the biological activity of fruits during storage. This research investigated the effect of exogenous melatonin (MT) on AsA metabolism in postharvest kiwifruit. Our results indicated that exogenous MT delayed the decrease of fruit firmness and titratable acid (TA), inhibited the increase of soluble solids content (SSC), reduced the respiration rate and ethylene production, and maintained a higher AsA content in kiwifruit during storage. The high expression of L-galactose pathway key genes in the early storage and regeneration genes in the later storage maintained the AsA content in postharvest kiwifruit. MT treatment enhanced the expression levels of AsA biosynthesis (AcGME2, AcGalDH, and AcGalLDH) and regeneration (AcGR, AcDHAR, and AcMDHAR1) genes. Meanwhile, the expression of the degradation gene AcAO was inhibited in MT-treated kiwifruits.</p

    Monosubstituted Benzene Derivatives from Fruits of Ficus hirta and Their Antifungal Activity against Phytopathogen Penicillium italicum

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    Ficus hirta, a widely consumed food by Hakka people, has been reported to show potent antifungal activity against phytopathogen Penicillium italicum. However, there is no report of chemical constituents responsible for the antifungal activity. In the current study, nine monosubstituted benzene derivatives, including three new derivatives (<b>1</b>–<b>3</b>), were isolated from the fruits of F. hirta. The structures of these isolates were elucidated on the basis of the analysis of spectroscopic data (mass spectrometry and nuclear magnetic resonance). All of the isolates were evaluated for antifungal activities against P. italicum. At an equivalent concentration, compound <b>1</b> exhibited stronger antifungal activity than that of the ethanol extract of F. hirta fruits

    Table_2_Red Light-Induced Systemic Resistance Against Root-Knot Nematode Is Mediated by a Coordinated Regulation of Salicylic Acid, Jasmonic Acid and Redox Signaling in Watermelon.DOCX

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    <p>Red light (RL) can stimulate plant defense against foliar diseases; however, its role in activation of systemic defense against root diseases remains unclear. Here, the effect of RL on root knot nematode Meloidogyne incognita (RKN) infestation was investigated in watermelon plants (Citrullus lanatus L.). Plants were exposed to 200 μmol m<sup>-2</sup> s<sup>-1</sup> photosynthetic photon flux density RL at the canopy level for 21 days using light-emitting photodiodes. The results showed that RL significantly suppressed gall formation and nematode development, which was closely associated with the RL-induced attenuation of oxidative stress in roots. Gene expression analysis showed that RL caused a transient upregulation of PR1 and WRKY70 transcripts at 7 days post inoculation in RKN-infected plants. Further investigation revealed that RL-induced systemic defense against RKN was attributed to increased jasmonic acid (JA) and salicylic acid (SA) content, and transcript levels of their biosynthetic genes in roots. Interestingly, while malondialdehyde content decreased, H<sub>2</sub>O<sub>2</sub> accumulation increased in RL-treated RKN-plants, indicating a potential signaling role of H<sub>2</sub>O<sub>2</sub> in mediating RL-induced systemic defense. Furthermore, analysis of enzymatic and non-enzymatic antidoxidants revealed that RL-induced enhanced defense agaist RKN was also attributed to increased activities of antioxidant enzymes as well as redox homeostasis. Taken together, these findings suggest that RL could enhance systemic resistance against RKN, which is mediated by a coordinated regulation of JA- and SA-dependent signaling, antioxidants, and redox homeostasis in watermelon plants.</p

    Table_1_Red Light-Induced Systemic Resistance Against Root-Knot Nematode Is Mediated by a Coordinated Regulation of Salicylic Acid, Jasmonic Acid and Redox Signaling in Watermelon.DOCX

    No full text
    <p>Red light (RL) can stimulate plant defense against foliar diseases; however, its role in activation of systemic defense against root diseases remains unclear. Here, the effect of RL on root knot nematode Meloidogyne incognita (RKN) infestation was investigated in watermelon plants (Citrullus lanatus L.). Plants were exposed to 200 μmol m<sup>-2</sup> s<sup>-1</sup> photosynthetic photon flux density RL at the canopy level for 21 days using light-emitting photodiodes. The results showed that RL significantly suppressed gall formation and nematode development, which was closely associated with the RL-induced attenuation of oxidative stress in roots. Gene expression analysis showed that RL caused a transient upregulation of PR1 and WRKY70 transcripts at 7 days post inoculation in RKN-infected plants. Further investigation revealed that RL-induced systemic defense against RKN was attributed to increased jasmonic acid (JA) and salicylic acid (SA) content, and transcript levels of their biosynthetic genes in roots. Interestingly, while malondialdehyde content decreased, H<sub>2</sub>O<sub>2</sub> accumulation increased in RL-treated RKN-plants, indicating a potential signaling role of H<sub>2</sub>O<sub>2</sub> in mediating RL-induced systemic defense. Furthermore, analysis of enzymatic and non-enzymatic antidoxidants revealed that RL-induced enhanced defense agaist RKN was also attributed to increased activities of antioxidant enzymes as well as redox homeostasis. Taken together, these findings suggest that RL could enhance systemic resistance against RKN, which is mediated by a coordinated regulation of JA- and SA-dependent signaling, antioxidants, and redox homeostasis in watermelon plants.</p
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