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A novel pathogenicity determinant hijacks maize catalase 1 to enhance viral multiplication and infection
Author(s) -
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
Publication year - 2021
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.17206
Subject(s) - biology , virology , nicotiana benthamiana , virus , ectopic expression , gene silencing , gene , genetics
Summary 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 ZmCAT s 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.