Yingying Wei

Tea tree oil exhibits antifungal activity against Botrytis cinerea by affecting mitochondria

In order to investigate the effects of tea tree oil (TTO) on mitochondrial morphology and function in Botrytis cinerea, mycelia were treated with TTO at different concentrations. TTO at 2ml/l severely damaged mitochondria, resulting in matrix loss and increased mitochondrial irregularity. Mitochondrial membrane permeability was increased by TTO, as evidenced by a decrease in intracellular adenosine triphosphate (ATP) content and an increase in extracellular ATP content. Increasing concentrations of TTO decreased the activities of enzymes related to mitochondrial function and the tricarboxylic acid (TCA) cycle, affecting malic dehydrogenase, succinate dehydrogenase, ATPase, citrate synthetase, isocitrate dehydrogenase and α-ketoglutarate dehydrogenase, while sharply increasing the level of reactive oxygen species (ROS). These results suggest that mitochondrial damage, resulting in the disruption of the TCA cycle and accumulation of ROS, is involved in the mechanism of TTO antifungal activity against B. cinerea.

Effects and possible mechanism of tea tree oil against Botrytis cinerea and Penicillium expansum in vitro and in vivo test

The purpose of this study was to investigate the antifungal activities and possible mechanisms of tea tree oil (TTO) against Botrytis cinerea and Penicillium expansum in vitro and in vivo. The results show that TTO exhibits dose-dependent antifungal activity against both pathogens, but P. expansum is less sensitive than B. cinerea to TTO not only in the in vitro test but also in artificially inoculated cherry fruits. TTO vapor treatment reduced the decay caused by these pathogens in inoculated cherry fruits, but the effect on P. expansum was less than that on B. cinerea. While the total lipid and ergosterol contents of the cell membrane are greater in P. expansum than in B. cinerea, TTO treatment lowers the total lipid content in the membranes of both species by well over 50%, and ergosterol content is reduced to a greater extent in B. cinerea than in P. expansum. In both pathogens, TTO alters mycelial morphology and cellular ultrastructure. Oxygen consumption measurements show that TTO inhibits respiratory metabolism via the tricarboxylic acid cycle pathway in both pathogens, though more severely in B. cinerea than in P. expansum. The relatively decreased sensitivity of P. expansum to TTO may be due to the fact that TTO causes less disruption of the cell membrane in this organism, and higher inhibition the respiratory metabolism to the extent observed in B. cinerea.

Metabolomic Analysis and Mode of Action of Metabolites of Tea Tree Oil Involved in the Suppression of Botrytis cinerea

Tea tree oil (TTO), a volatile essential oil, has been widely used as an antimicrobial agent. However, the mechanism underlying TTO antifungal activity is not fully understood. In this study, a comprehensive metabolomics survey was undertaken to identify changes in metabolite production in Botrytis cinerea cells treated with TTO. Significant differences in 91 metabolites were observed, including 8 upregulated and 83 downregulated metabolites in TTO-treated cells. The results indicate that TTO inhibits primary metabolic pathways through the suppression of the tricarboxylic acid (TCA) cycle and fatty acid metabolism. Further experiments show that TTO treatment decreases the activities of key enzymes in the TCA cycle and increases the level of hydrogen peroxide (H2O2). Membrane damage is also induced by TTO treatment. We hypothesize that the effect of TTO on B. cinerea is achieved mainly by disruption of the TCA cycle and fatty acid metabolism, resulting in mitochondrial dysfunction and oxidative stress.

Hot Air Treatment Induces Disease Resistance through Activating the Phenylpropanoid Metabolism in Cherry Tomato Fruit

To explore the effects of hot air (HA, 38 °C for 12 h) treatment on the phenylpropanoid metabolism in cherry tomatoes, phenylpropanoid metabolite levels and the activities and expression of key enzymes were analyzed in HA-treated fruit. HA treatment enhanced phenylpropanoid metabolism, as evidenced by elevated levels of phenolics and flavonoids, higher activities of phenylalanine ammonia-lyase and cinnamate-4-hydroxylase, and upregulated expression of LeCHS, LeCHI, LeF3H, and LeFLS. Levels of several phenylpropanoid metabolites were higher after HA treatment, including p-coumaric acid, caffeic acid, chlorogenic acid, isoquercitrin, quercetin, and rutin. These metabolic changes may be related to the reduced disease incidence and smaller lesion diameters observed in HA-treated fruit inoculated with Alternaria alternata (black mold) or Botrytis cinerea (gray mold). The results suggest that HA treatment induces disease resistance by activating the phenylpropanoid pathway in cherry tomato fruit.

Hot air treatment reduces postharvest decay and delays softening of cherry tomato by regulating gene expression and activities of cell wall‐degrading enzymes

BACKGROUND Fruit softening facilitates pathogen infection and postharvest decay, leading to the reduction of shelf-life. Hot air (HA) treatment at 38 °C for 12 h is effective in reducing postharvest disease and chilling injury of tomato fruit. To explore the effect and mechanism of HA treatment on reducing postharvest decay and softening of cherry tomato, fruit at the mature green stage were treated with HA and then stored at 20 °C for 15 days. Changes in natural decay incidence, firmness, cell wall compositions, activities and gene expression of cell wall-degrading enzymes of cherry tomatoes were assessed. RESULTS HA treatment reduced natural decay incidence, postponed the firmness decline, inhibited the respiration rate and ethylene production, and retarded pectin solubilisation and cellulose degradation of cherry tomatoes. Enzymatic activities and gene expression of pectin methylesterase, polygalacturonase, cellulase and β-galactosidase were inhibited by HA treatment. In addition, the gene expression of LeEXP1 was reduced, while LeEXT was up-regulated after HA treatment. CONCLUSIONS Our findings suggested that HA treatment could inhibit cell wall degradation and postpone softening of cherry tomatoes by regulating gene expression and activities of cell wall-degrading enzymes, resulting in the reduction of postharvest decay.

Rapid detection of adulterated peony seed oil by electronic nose

Peony seed oil has recently been introduced as a high-quality food oil. Because the high price of peony seed oil may tempt unscrupulous merchants to dilute it with cheaper substitutes, a rapid detection method for likely adulterants is required. In this study, the fatty acid composition of peony seed oil and four less expensive edible oils (soybean oil, corn oil, sunflower oil, and rapeseed oil) were measured by gas chromatography mass spectrometry. Peony oil adulterated by other edible oils was assessed using iodine values to estimate the extent of adulteration. Adulteration was also measured using an electronic nose (E-nose) combined with principal component analysis (PCA) or linear discriminant analysis (LDA). Results indicated that peony seed oil was highly enriched in α-linolenic acid. Although the iodine value can be used to detect some adulterants by measuring unsaturation, it was not able to detect all four potential adulterants. In contrast, the E-nose can rapidly identify adulterated peony seed oil by sampling vapor. Data analyses using PCA and LDA show that LDA more effectively clusters the data, discriminates between pure and adulterated oil, and can detect adulteration at the 10% level. E-nose combined with LDA suitable for detection of peony seed oil adulteration.

Infection of post-harvest peaches by Monilinia fructicola accelerates sucrose decomposition and stimulates the Embden–Meyerhof–Parnas pathway

To study the changes in sugar metabolism caused by fungal infection in post-harvest peaches, fruit from two cultivars (‘Baifeng’ and ‘Yulu’) was inoculated with Monilinia fructicola and stored at 10 °C. During disease development, soluble sugar content was monitored, as well as the activities and expression of selected enzymes. Disease progression was accompanied by a decrease in sucrose content and increases in reducing sugars and soluble solids, consistent with higher enzyme activities for acid invertase, neutral invertase and sucrose synthase-cleavage, and lower activities for sucrose synthase-synthesis and sucrose phosphate synthase. Activities of phosphofructokinase, hexokinase, and pyruvate kinase, which are related to hexose metabolism, also increased. These changes stimulate the Embden–Meyerhof–Parnas (EMP) pathway. We conclude that the fungal disease in peach fruit accelerates the decomposition of sucrose, thereby providing more glucose as a substrate to the EMP pathway.Fruit fungal infection: Effects on sugar metabolismA study by researchers in China provides insights into changes to sugar metabolism during fungal infection in post-harvest peaches. Fungal infections and associated disease development can alter sugar metabolism in post-harvest fruits, leading to rapid decay and a short shelf life. However, little is known about the mechanisms behind these fungal infections. Xingfeng Shao and Yingying Wei at Ningbo University and co-workers examined the effect of brown rot, caused by a fungus called Monilinia fructicola, on sugar metabolism in two peach cultivars kept under chilled conditions. As the disease progressed, the fruit increased its energy supply by decomposing sucrose and generating more glucose. The team uncovered the major enzymes responsible for this sucrose decomposition. The increased glucose stimulated the Embden-Meyerhof-Parnas pathway, which in turn helped the peaches fight infection.

iTRAQ Proteomic Analysis Reveals That Metabolic Pathways Involving Energy Metabolism Are Affected by Tea Tree Oil in Botrytis cinerea

Tea tree oil (TTO) is a volatile essential oil obtained from the leaves of the Australian tree Melaleuca alternifolia by vapor distillation. Previously, we demonstrated that TTO has a strong inhibitory effect on Botrytis cinerea. This study investigates the underlying antifungal mechanisms at the molecular level. A proteomics approach using isobaric tags for relative and absolute quantification (iTRAQ) was adopted to investigate the effects of TTO on B. cinerea. A total of 718 differentially expression proteins (DEPs) were identified in TTO-treated samples, 17 were markedly up-regulated and 701 were significantly down-regulated. Among the 718 DEPs, 562 were annotated and classified into 30 functional groups by GO (gene ontology) analysis. KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment analysis linked 562 DEPs to 133 different biochemical pathways, involving glycolysis, the tricarboxylic acid cycle (TCA cycle), and purine metabolism. Additional experiments indicated that TTO destroys cell membranes and decreases the activities of three enzymes related to the TCA cycle. Our results suggest that TTO treatment inhibits glycolysis, disrupts the TCA cycle, and induces mitochondrial dysfunction, thereby disrupting energy metabolism. This study provides new insights into the mechanisms underlying the antifungal activity of essential oils.