The mechanism of induced resistance against Fusarium dry rot in potato tubers by the T-2 toxin

Xue, Huali; Bi, Yang; Prusky, Dov; Hussain, Raza; Zhang, Rui; Zhang, Shan; Nan, Mina; Zong, Yuanyuan; Cheng, Xiaoyan

doi:10.1016/j.postharvbio.2019.03.021

Cited by 16 publications

(12 citation statements)

References 39 publications

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“…Chitosan films are also effective gas barriers, which modifies fruit’s internal atmosphere by controlling the supply of O 2 , CO 2 , and moisture, thus reducing water transpiration and respiration and delaying ripening and senescence of fruits, which was evident in sweet cherries, strawberries, and pomegranates during storage ( Pasquariello et al, 2015 ; Petriccione et al, 2015 ; Varasteh et al, 2017 ). In addition, lignin accumulation limits fruit water evaporation when formed on a wounded surface ( Xue et al, 2019 ). Thus, the gradual accretion of lignin at the wound site of fruit in the present study also reduced water loss.…”

Section: Discussionmentioning

confidence: 99%

“…Monolignins ( p -coumaryl alcohol, coniferyl alcohol, and sinapyl alcohol) are polymerized into p -hydroxyphenyl lignin, guaiacol lignin, and syringyl lignin linked by ether bonds into a structure known as polymer lignin, which is strong enough to prevent pathogen invasion ( Yang et al, 2020 ; Zhu et al, 2021 ). Moreover, lignin accumulation is known to limit water evaporation and restrict pathogen infections ( Xue et al, 2019 ). Our results show that chitosan treatment enhanced the synthesis of p -coumaryl alcohol, coniferyl alcohol, and sinapyl alcohol, which accumulated into lignin ( Figure 5 ).…”

Section: Discussionmentioning

confidence: 99%

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Chitosan Treatment Promotes Wound Healing of Apple by Eliciting Phenylpropanoid Pathway and Enzymatic Browning of Wounds

et al. 2022

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Chitosan is an elicitor that induces resistance in fruits against postharvest diseases, but there is little knowledge about the wound healing ability of chitosan on apple fruits. Our study aimed at revealing the effect of chitosan on the phenylpropanoid pathway by determining some enzyme activities, products metabolites, polyphenol oxidase activity, color (L*, b*, a*), weight loss, and disease index during healing. Apple (cv. Fuji) fruits wounded artificially were treated with 2.5% chitosan and healed at 21–25°C, relative humidity = 81–85% for 7 days, and non-wounded fruits (coated and non-coated) were used as control. The result shows that chitosan treatment significantly decreased weight loss of wounded fruits and disease index of Penicillium expansum inoculated fruits. The activities of phenylalanine ammonia-lyase (PAL), cinnamic acid 4-hydroxylase (C4H), 4-coumaryl coenzyme A ligase (4CL), cinnamoyl-CoA reductase (CCR), and cinnamyl alcohol dehydrogenase (CAD) were elicited throughout the healing period by chitosan, which increased the biosynthesis of cinnamic acid, caffeic acid, ferulic acid, sinapic acid, p-coumaric acid, p-coumaryl alcohol, coniferyl alcohol, and sinapyl alcohol. Also, total phenol, flavonoid, and lignin contents were significantly increased at the fruits wounds. In addition, chitosan’s ability to enhance polyphenol oxidase activity stimulated enzymatic browning of wounds. Although wounding increased phenylpropanoid enzymes activities before healing, chitosan caused higher enzyme activities for a significant healing effect compared with the control. These findings imply that chitosan accelerates apple wound healing by activating the phenylpropanoid pathway and stimulating enzymatic browning of wounds.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Chitosan Treatment Promotes Wound Healing of Apple by Eliciting Phenylpropanoid Pathway and Enzymatic Browning of Wounds

et al. 2022

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“…The quest of finding some bioagents and chemicals for induced resistance led to the finding of T2-Toxin produced by Fusarium species which developed inherent resistance in potato against F. sulphureum. The T2-Toxin (1 mg L −1 ) with its elicitor like activity enhanced the production of ROS and new phenylpropanoid metabolites (Xue et al 2019).…”

Section: Biological Controlmentioning

confidence: 99%

Potato dry rot disease: current status, pathogenomics and management

et al. 2020

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Potato dry rot disease caused by Fusarium species is a major threat to global potato production. The soil and seed-borne diseases influence the crop stand by inhibiting the development of potato sprouts and cause severe rots in seed tubers, table and processing purpose potatoes in cold stores. The symptoms of the dry rot include sunken and wrinkled brown to black tissue patches on tubers having less dry matter and shriveled flesh. Fungal infection accompanied by toxin development in the rotten tubers raises more concern for consumer health. The widespread dry rot causing fungal species (Fusarium graminearum) is reported to have a hemibiotrophic lifestyle. A cascade of enzymes, toxins and small secreted proteins are involved in the pathogenesis of these hemibiotrophs. With the availability of the genome sequence of the most devastating species Fusarium sambucinum, it is important to identify the potential pathogenicity factors and small secreted proteins that will help in designing management strategies. Limited resistant cultivars and the emergence of fungicide-resistant strains have made it more threatening for potato cultivation and trade. Several novel fungicide molecules (Azoxystrobin, chlorothalonil and fludioxonil), are found very effective as tuber treatment chemicals. Besides, many beneficial bioagents and safer chemicals have shown antibiosis and mycoparasitism against this pathogen. Germplasm screening for dry rot resistance is important to assist the resistance breeding program for the development of resistant cultivars. This review aims to draw attention to the symptomatology, infection process, pathogenomics, the role of toxins and management approaches for potato dry rot disease, which is very much critical in designing better management strategies.

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“…In plants, immunoprotective effects of T-2 were also reported. The mechanism of resistance to Fusarium dry rot induced by T-2 in potato tubers includes reactive oxygen species (ROS) activation and phenylpropanoid metabolism (Xue et al 2019).…”

Section: Immunotoxicity Mechanisms Of T-2 Toxin Immunotoxicitymentioning

confidence: 99%

An update on T-2 toxin and its modified forms: metabolism, immunotoxicity mechanism, and human exposure assessment

Qin

Kuča

et al. 2020

Arch Toxicol

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T-2 toxin is the most toxic trichothecene mycotoxin, and it exerts potent toxic effects, including immunotoxicity, neurotoxicity, and reproductive toxicity. Recently, several novel metabolites, including 3′,4′-dihydroxy-T-2 toxin and 4′,4′-dihydroxy-T-2 toxin, have been uncovered. The enzymes CYP3A4 and carboxylesterase contribute to T-2 toxin metabolism, with 3′-hydroxy-T-2 toxin and HT-2 toxin as the corresponding primary products. Modified forms of T-2 toxin, including T-2-3-glucoside, exert their immunotoxic effects by signaling through JAK/STAT but not MAPK. T-2-3-glucoside results from hydrolyzation of the corresponding parent mycotoxin and other metabolites by the intestinal microbiota, which leads to enhanced toxicity. Increasing evidence has shown that autophagy, hypoxia-inducible factors, and exosomes are involved in T-2 toxin-induced immunotoxicity. Autophagy promotes the immunosuppression induced by T-2 toxin, and a complex crosstalk between apoptosis and autophagy exists. Very recently, "immune evasion" activity was reported to be associated with this toxin; this activity is initiated inside cells and allows pathogens to escape the host immune response. Moreover, T-2 toxin has the potential to trigger hypoxia in cells, which is related to activation of hypoxia-inducible factor and the release of exosomes, leading to immunotoxicity. Based on the data from a series of human exposure studies, free T-2 toxin, HT-2 toxin, and HT-2-4-glucuronide should be considered human T-2 toxin biomarkers in the urine. The present review focuses on novel findings related to the metabolism, immunotoxicity, and human exposure assessment of T-2 toxin and its modified forms. In particular, the immunotoxicity mechanisms of T-2 toxin and the toxicity mechanism of its modified form, as well as human T-2 toxin biomarkers, are discussed. This work will contribute to an improved understanding of the immunotoxicity mechanism of T-2 toxin and its modified forms. Keywords T-2 toxin • Modified T-2 toxin • Metabolism • Immunotoxicity • Human exposure assessments • Biomarkers Abbreviations AhR Aryl hydrocarbon receptor AKNA AT-hook transcriptionfactor Akt Serine/threonine protein kinase ARE Antioxidant response element CREB CAMP-response clement-binding protein CYP450 Cytochrome P450 DAS Diacetoxyscirpenol DRP-1 Dynamin-related protein 1 DON Deoxynivalenol D3G Deoxynivalenol-3-glucoside ECM Extracellular matrix EIF2AK2 Double-stranded RNA-activated protein kinase ERK Etracellular signaling kinase FXR Farnesoid X receptor GH Growth hormone Qinghua Wu and Zihui Qin contributed equally to this work.

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The mechanism of induced resistance against Fusarium dry rot in potato tubers by the T-2 toxin

Cited by 16 publications

References 39 publications

Chitosan Treatment Promotes Wound Healing of Apple by Eliciting Phenylpropanoid Pathway and Enzymatic Browning of Wounds

Chitosan Treatment Promotes Wound Healing of Apple by Eliciting Phenylpropanoid Pathway and Enzymatic Browning of Wounds

Potato dry rot disease: current status, pathogenomics and management

An update on T-2 toxin and its modified forms: metabolism, immunotoxicity mechanism, and human exposure assessment

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