Hashimoto Masayoshi, Komatsu Ken, Iwai Ryo, Keima Takuya, Maejima Kensaku, Shiraishi Takuya, Ishikawa Kazuya, Yoshida Tetsuya, Kitazawa Yugo, Okano Yukari, Yamaji Yasuyuki, Namba Shigetou
1 Laboratory of Plant Pathology, Department of Agricultural and Environmental Biology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan;
2 Laboratory of Plant Pathology, Tokyo University of Agriculture and Technology (TUAT), 3-5-8 Saiwaicho, Fuchu, Tokyo 183-8509, Japan.
Mol Plant Microbe Interact. 2015 Jun;28(6):675-88. doi: 10.1094/MPMI-01-15-0004-R. Epub 2015 Jun 12.
Systemic necrosis is one of the most severe symptoms caused by plant RNA viruses. Recently, systemic necrosis has been suggested to have similar features to a defense response referred to as the hypersensitive response (HR), a form of programmed cell death. In virus-infected plant cells, host intracellular membrane structures are changed dramatically for more efficient viral replication. However, little is known about whether this replication-associated membrane modification is the cause of the symptoms. In this study, we identified an amino-terminal amphipathic helix of the helicase encoded by Radish mosaic virus (RaMV) (genus Comovirus) as an elicitor of cell death in RaMV-infected plants. Cell death caused by the amphipathic helix had features similar to HR, such as SGT1-dependence. Mutational analyses and inhibitor assays using cerulenin demonstrated that the amphipathic helix-induced cell death was tightly correlated with dramatic alterations in endoplasmic reticulum (ER) membrane structures. Furthermore, the cell death-inducing activity of the amphipathic helix was conserved in Cowpea mosaic virus (genus Comovirus) and Tobacco ringspot virus (genus Nepovirus), both of which are classified in the family Secoviridae. Together, these results indicate that ER membrane modification associated with viral intracellular replication may be recognized to prime defense responses against plant viruses.
系统性坏死是植物RNA病毒引起的最严重症状之一。最近,有人提出系统性坏死具有与一种称为过敏反应(HR)的防御反应相似的特征,HR是一种程序性细胞死亡形式。在病毒感染的植物细胞中,宿主细胞内膜结构会发生显著变化,以实现更高效的病毒复制。然而,对于这种与复制相关的膜修饰是否是症状的原因,人们知之甚少。在本研究中,我们鉴定出萝卜花叶病毒(RaMV,豇豆花叶病毒属)编码的解旋酶的氨基末端两亲性螺旋作为RaMV感染植物中细胞死亡的激发子。由两亲性螺旋引起的细胞死亡具有与HR相似的特征,如依赖SGT1。使用浅蓝菌素进行的突变分析和抑制剂试验表明,两亲性螺旋诱导的细胞死亡与内质网(ER)膜结构的显著改变密切相关。此外,两亲性螺旋的细胞死亡诱导活性在豇豆花叶病毒(豇豆花叶病毒属)和烟草环斑病毒(线虫传多面体病毒属)中保守,这两种病毒都属于矮化病毒科。总之,这些结果表明,与病毒细胞内复制相关的ER膜修饰可能被识别为引发针对植物病毒的防御反应。