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α–苦瓜素基因提高番茄对烟草花叶病毒抗性的机理研究

Studies on the Mechanism of α-Momordicin Gene Enhancing Tomato Resistance to Tobacco Mosaic Virus
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摘要 为了深入探究α–苦瓜素基因(αMMC)抗烟草花叶病毒(TMV)的机理,利用“番茄—TMV”互作系统,分析了αMMC转基因植株和野生型植株的生理生化参数及防御相关基因的表达。结果表明,αMMC为Ⅰ型核糖体失活蛋白,定位于细胞质;αMMC可以抑制病毒在寄主体内的繁殖,减轻番茄的病害症状,正调控番茄的防御系统。TMV侵染引起寄主体内活性氧的爆发,αMMC可以增强抗氧化酶的活性以清除活性氧,降低植物的氧化损伤,维持细胞内的氧化平衡。RT-qPCR检测结果表明,αMMC能特异性诱导防御相关基因PR1、PR4、PR6和PRB1-3的表达以提高寄主抵御TMV侵染的能力。 To explore the mechanism ofα-momordicin(αMMC)resistance to tobacco mosaic virus(TMV),the physiological parameters,virus accumulation,and the transcript levels of pathogenesis-related protein(PR)gene inαMMC transgenic plants and wild-type plants under TMV inoculation were analyzed using the‘tomato-TMV’interaction system.Subcellular localization and phenotypic analysis showed thatαMMC was a type I ribosome-inactivating protein and localized in the cytoplasm.Furthermore,αMMC could inhibit virus accumulation in the host and alleviate the disease symptoms in tomato,positively the plant’s defense system.Oxidative damage and enzyme activity assays showed that TMV infection caused an outbreak of reactive oxygen species,andαMMC could enhance the activities of antioxidant enzyme to remove excessive reactive oxygen species,resulting in less oxidative damage.In addition,real-time quantitative PCR results indicated thatαMMC could specifically induce the expression level of defense-related genes PR1,PR4,PR6 and PRB1-3 to improve host resistance to TMV infection.
作者 杨婷 席德慧 夏明 李佳楠 YANG Ting;XI Dehui;XIA Ming;LI Jianan(Hubei Engineering Research Center for Protection and Utilization of Special Biological Resources in the Hanjiang River Basin,College of Life Sciences,Jianghan University,Wuhan 430056,China;Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education,College of Life Sciences,Sichuan University,Chengdou 610065,China)
出处 《园艺学报》 CAS CSCD 北大核心 2024年第5期1126-1136,共11页 Acta Horticulturae Sinica
基金 湖北省自然科学基金项目(2022CFB909) 国家自然科学基金青年基金项目(31900095)。
关键词 番茄 α–苦瓜素 TMV 抗性机理 氧化损伤 tomato α-momorcharin tobacco mosaic virus resistance mechanism oxidative damage
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