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Identification of differentially regulated maize proteins conditioning Sugarcane mosaic virus systemic infection
Author(s) -
Chen Hui,
Cao Yanyong,
Li Yiqing,
Xia Zihao,
Xie Jipeng,
Carr John P.,
Wu Boming,
Fan Zaifeng,
Zhou Tao
Publication year - 2017
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.14645
Subject(s) - brome mosaic virus , biology , gene , gene knockdown , virus , potato virus x , gene silencing , viral replication , cucumber mosaic virus , plant disease resistance , protein disulfide isomerase , plant virus , genetics , virology , rna , rna dependent rna polymerase , endoplasmic reticulum
SummarySugarcane mosaic virus ( SCMV ) is the most important cause of maize dwarf mosaic disease. To identify maize genes responsive to SCMV infection and that may be involved in pathogenesis, a comparative proteomic analysis was performed using the first and second systemically infected leaves (termed 1 SL and 2 SL , respectively). Seventy‐one differentially expressed proteins were identified in 1 SL and 2 SL upon SCMV infection. Among them, eight proteins showed the same changing patterns in both 1 SL and 2 SL . Functional annotations of regulated proteins and measurement of photosynthetic activity revealed that photosynthesis was more inhibited and defensive gene expression more pronounced in 1 SL than in 2 SL . Knockdown of regulated proteins in both 1 SL and 2 SL by a brome mosaic virus‐based gene silencing vector in maize indicated that protein disulfide isomerase‐like and phosphoglycerate kinase were required for optimal SCMV replication. By contrast, knockdown of polyamine oxidase (Zm PAO ) significantly increased SCMV accumulation, implying that Zm PAO activity might contribute to resistance or tolerance. The results suggest that combining comparative proteomic analyses of different tissues and virus‐induced gene silencing is an efficient way to identify host proteins supporting virus replication or enhancing resistance to virus infection.