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一种新型致病性决定因素劫持玉米过氧化氢酶1以增强病毒增殖和感染。

A novel pathogenicity determinant hijacks maize catalase 1 to enhance viral multiplication and infection.

作者信息

Jiao Zhiyuan, Tian Yiying, Cao Yanyong, Wang Juan, Zhan Binhui, Zhao Zhenxing, Sun Biao, Guo Chang, Ma Wendi, Liao Zhenfeng, Zhang Hengmu, Zhou Tao, Xia Yiji, Fan Zaifeng

机构信息

State Kay Laboratory of Agrobiotechnology and Key Laboratory of Pest Monitoring and Green Management-MOA, Department of Plant Pathology, China Agricultural University, Beijing, 100193, China.

Cereal Crops Institute, Henan Academy of Agricultural Sciences, Zhengzhou, 450002, China.

出版信息

New Phytol. 2021 May;230(3):1126-1141. doi: 10.1111/nph.17206. Epub 2021 Feb 24.

DOI:10.1111/nph.17206
PMID:33458828
Abstract

Pathogens have evolved various strategies to overcome host immunity for successful infection. Maize chlorotic mottle virus (MCMV) can cause lethal necrosis in maize (Zea mays) when it coinfects with a virus in the Potyviridae family. However, the MCMV pathogenicity determinant remains largely unknown. Here we show that the P31 protein of MCMV is important for viral accumulation and essential for symptom development. Ectopic expression of P31 using foxtail mosaic virus or potato virus X induced necrosis in systemically infected maize or Nicotiana benthamiana leaves. Maize catalases (CATs) were shown to interact with P31 in yeast and in planta. P31 accumulation was elevated through its interaction with ZmCAT1. P31 attenuated the expression of salicylic acid (SA)-responsive pathogenesis-related (PR) genes by inhibiting catalase activity during MCMV infection. In addition, silencing of ZmCATs using a brome mosaic virus-based gene silencing vector facilitated MCMV RNA and coat protein accumulation. This study reveals an important role for MCMV P31 in counteracting host defence and inducing systemic chlorosis and necrosis. Our results have implications for understanding the mechanisms in defence and counter-defence during infection of plants by various pathogens.

摘要

病原体已经进化出各种策略来克服宿主免疫以成功感染。玉米褪绿斑驳病毒(MCMV)与马铃薯Y病毒科的一种病毒共同感染时可在玉米(Zea mays)中引起致死性坏死。然而,MCMV的致病性决定因素在很大程度上仍不清楚。在此我们表明,MCMV的P31蛋白对病毒积累很重要,对症状发展必不可少。利用狐尾花叶病毒或马铃薯X病毒异位表达P31会在系统感染的玉米或本氏烟草叶片中诱导坏死。已证明玉米过氧化氢酶(CATs)在酵母和植物中与P31相互作用。通过与ZmCAT1相互作用,P31的积累增加。在MCMV感染期间,P31通过抑制过氧化氢酶活性来减弱水杨酸(SA)响应的病程相关(PR)基因的表达。此外,使用基于雀麦花叶病毒的基因沉默载体沉默ZmCATs促进了MCMV RNA和外壳蛋白的积累。本研究揭示了MCMV P31在对抗宿主防御以及诱导系统性萎黄和坏死中的重要作用。我们的结果对于理解各种病原体感染植物期间防御和反防御机制具有重要意义。

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