Overexpression of NtERF5, belonging to the ethylene response factor gene family, inhibits potato virus X infection and enhances expression of jasmonic acid/ethylene signaling marker genes in tobacco

被引:0
作者
Hiyori Suzuki
Tomoki Ito
Takuya Ogata
Yuki Tsukahara
Richard S. Nelson
Nobumitsu Sasaki
Yasuhiko Matsushita
机构
[1] Tokyo University of Agriculture and Technology (TUAT),Gene Research Center
[2] Tokyo University of Agriculture and Technology (TUAT),Graduate School of Agricultural Science
[3] Japan International Research Center for Agricultural Sciences (JIRCAS),Biological Resources and Post
[4] Oklahoma State University,Harvest Division
[5] Tokyo University of Agriculture and Technology,Department of Entomology & Plant Pathology
来源
Journal of General Plant Pathology | 2024年 / 90卷
关键词
Ethylene response factor; Potato virus X; Virus resistance; Pathogenesis-related protein; SHE1;
D O I
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中图分类号
学科分类号
摘要
Transcription factors belonging to the family of ethylene response factors (ERFs) in plants function in disease resistance to pathogens. One of the tobacco ERF genes, NtERF5, inhibits the accumulation of tobacco mosaic virus (genus Tobamovirus) when overexpressed in tobacco carrying the resistance gene N. Here, we report that NtERF5 can function as a transcriptional activator through binding of the GCC-box in planta. We then determined whether overexpression of NtERF5 in tobacco lacking the N gene (nn tobacco) inhibited infection by potato virus X (PVX: genus Potexvirus). Transient overexpression of NtERF5 inhibited the accumulation of PVX without affecting virus spread and increased the transcript levels of NtPRB-1b and NtPR6, which are jasmonic acid/ethylene-signaling marker genes encoding pathogenesis-related (PR) proteins. Stable overexpression of NtERF5 in nn tobacco also resulted in decreased PVX accumulation and the induction of the expression of NtPRB-1b and NtPR6. Our results revealed that overexpression of NtERF5 limited successful infection and accumulation of PVX, suggesting the role of NtERF5 as a positive regulator of basal defense against virus infection.
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页码:125 / 133
页数:8
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