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The coat protein p25 from maize chlorotic mottle virus involved in symptom development and systemic movement of tobacco mosaic virus hybrids

文献类型： 外文期刊

作者： Zhang, Chao 1 ; Wang, Di 2 ; Li, Weimin 3 ; Zhang, Baolong 4 ; Abdel-Fattah Ouf, Gamal M. 5 ; Su, Xiaofeng 3 ; Li, Jun 1 ;

作者机构： 1.Hebei Agr Univ, Coll Life Sci, State Key Lab North China Crop Improvement & Regul, Baoding, Peoples R China

2.Natl Inst Metrol, Ctr Adv Measurement Sci, Beijing, Peoples R China

3.Chinese Acad Agr Sci, Biotechnol Res Inst, Beijing, Peoples R China

4.Jiangsu Acad Agr Sci, Excellence & Innovat Ctr, Nanjing, Peoples R China

5.Mansoura Univ, Fac Sci, Dept Bot & Appl Microbiol, Mansoura, Egypt

关键词： MCMV; p25; pathogenicity; systemic movement; HSP90

期刊名称：FRONTIERS IN MICROBIOLOGY （ 影响因子：6.064； 五年影响因子：6.843 ）

ISSN：

年卷期： 2022 年 13 卷

页码：

收录情况： SCI

摘要： Viral coat protein (CP) has numerous critical functions in plant infection, but little is known about p25, the CP of maize chlorotic mottle virus (MCMV; Machlomovirus), which causes severe yield losses in maize worldwide. Here, we investigated the roles of p25 in pathogenicity and systemic movement, as well as potential interactions with host plants, using a hybrid tobacco mosaic virus (TMV)-based expression system. Highly conserved protein p25 is predicted to contain a membrane-anchored nuclear localization signal (NLS) sequence and an extracellular sequence. In transgenic Nicotiana benthamiana plants containing the movement protein (MP) of TMV (TMV-MP), p25 induced severe symptoms, including dwarf and foliar necrosis, and was detected in inoculated and non-inoculated leaves. After the deletion of NLS from nuclear-located p25, the protein was found throughout the host cell, and plant stunting and starch granule deformity were reduced. Systemic movement and pathogenicity were significantly impaired when the C-terminal regions of p25 were absent. Using virus-induced gene silencing (VIGS), the transcript level of heat shock protein HSP90 was distinctly lower in host plants in association with the absence of leaf necrosis induced by TMV-p25. Our results revealed crucial roles for MCMV p25 in viral pathogenicity, long-distance movement, and interactions with N. benthamiana.

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