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高温下烟草中烟草花叶病毒诱导的过敏型坏死的抑制与NADPH氧化酶和超氧化物的下调以及脱氢抗坏血酸还原酶的刺激有关。

Suppression of tobacco mosaic virus-induced hypersensitive-type necrotization in tobacco at high temperature is associated with downregulation of NADPH oxidase and superoxide and stimulation of dehydroascorbate reductase.

作者信息

Király L, Hafez Y M, Fodor J, Király Z

机构信息

Plant Protection Institute, Hungarian Academy of Sciences, PO Box 102, H-1525 Budapest, Hungary.

Department of Botany, Plant Pathology Branch, Faculty of Agriculture, Kafr-El-Sheikh University, Kafr-El-Sheikh, Egypt.

出版信息

J Gen Virol. 2008 Mar;89(Pt 3):799-808. doi: 10.1099/vir.0.83328-0.

DOI:10.1099/vir.0.83328-0
PMID:18272772
Abstract

Tissue necroses and resistance during the hypersensitive response (HR) of tobacco to tobacco mosaic virus (TMV) are overcome at temperatures above 28 degrees C and the virus multiplies to high levels in the originally resistant N-gene expressing plants. We have demonstrated that chemical compounds that generate reactive oxygen species (ROS) or directly applied hydrogen peroxide (H(2)O(2)) are able to induce HR-type necroses in TMV-inoculated Xanthi-nc tobacco even at high temperatures (e.g. 30 degrees C). The amount of superoxide (O(2)(*-)) decreased, while H(2)O(2) slightly increased in TMV- and mock-inoculated leaves at 30 degrees C, as compared with 20 degrees C. Activity of NADPH oxidase and mRNA levels of genes that encode NADPH oxidase and an alternative oxidase, respectively, were significantly lower, while activity of dehydroascorbate reductase was significantly higher at 30 degrees C, as compared with 20 degrees C. It was possible to reverse or suppress the chemically induced HR-type necrotization at 30 degrees C by the application of antioxidants, such as superoxide dismutase and catalase, demonstrating that the development of HR-type necroses indeed depends on a certain level of superoxide and other ROS. Importantly, high TMV levels at 30 degrees C were similar in infected plants, whether the HR-type necrotization developed or not. Suppression of virus multiplication in resistant, HR-producing tobacco at lower temperatures seems to be independent of the appearance of necroses but is associated with temperatures below 28 degrees C.

摘要

烟草对烟草花叶病毒(TMV)过敏反应(HR)期间的组织坏死和抗性在28摄氏度以上的温度下会被克服,并且病毒会在原本具有抗性的N基因表达植物中大量繁殖。我们已经证明,即使在高温(例如30摄氏度)下,能够产生活性氧(ROS)的化合物或直接施加的过氧化氢(H₂O₂)也能够在接种TMV的Xanthi-nc烟草中诱导HR型坏死。与20摄氏度相比,在30摄氏度下接种TMV和模拟接种的叶片中,超氧阴离子(O₂⁻·)的量减少,而H₂O₂略有增加。与20摄氏度相比,30摄氏度时NADPH氧化酶的活性以及分别编码NADPH氧化酶和交替氧化酶的基因的mRNA水平显著降低,而脱氢抗坏血酸还原酶的活性显著升高。通过应用抗氧化剂,如超氧化物歧化酶和过氧化氢酶,可以在30摄氏度下逆转或抑制化学诱导的HR型坏死,这表明HR型坏死的发展确实取决于一定水平的超氧阴离子和其他ROS。重要的是,无论是否发生HR型坏死,在30摄氏度下感染植物中的TMV高水平相似。在较低温度下抑制抗性、产生HR的烟草中的病毒繁殖似乎与坏死的出现无关,但与低于28摄氏度的温度有关。

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