Molecular Plant-Virus Interactions: Defense and Counter-defense

病毒性病原体占新发病例的比例最大 植物病害，威胁全球粮食安全。为了对抗病毒植物 已经进化出了复杂的防御机制作为回应，病毒也 进化出了抵抗宿主防御的毒力策略。的长期目标 我们的研究计划是了解复杂的病毒-植物相互作用， 特别是病毒和植物之间的共同进化军备竞赛， 开发新技术控制病毒性疾病， 作物生产。越来越多的证据表明，RNA靶向 免疫，包括RNA沉默，RNA衰变和RNA质量控制， 调节内源性基因表达，是病毒病原体的核心防御 在植物中。这些RNA免疫途径可能以分级和协调的方式起作用。 以RNA沉默作为主要参与者来抑制病毒感染的模式。RNA 由双链RNA触发的沉默，是一种基本的， 序列特异性机制在所有真核生物中保守。病毒编码病毒 RNA沉默抑制子（VSRs），与细胞因子结合， RNA沉默。最近，我们发现VSRs也通过以下方式破坏RNA衰变： 与关键细胞衰变途径组分的相互作用， 感染和自噬起着相反的作用（主要是抗病毒）， 病毒感染通过调节VSRs。由于VSR序列高度多样， 它们似乎与宿主蛋白质相互作用以执行其功能。在这 建议的研究，我们将确定宿主蛋白，通过招募 与VSR相互作用，特异性发挥RNA靶向抗病毒作用 免疫力而不是内源性基因调控。我们将进一步描述 它们在抗性信号通路中的机制细节，并阐明 病毒干扰这些细胞因子的抗病毒功能 使用经典的分子和细胞生物学技术。另一 新出现的关键抗病毒防御是宿主因子介导的隐性抗性。 绝大多数植物病毒都有一个小的正义单链 RNA基因组具有非常有限的编码能力。因此，入侵病毒依赖于 对一些宿主因素，以建立其感染和破坏的 宿主因子-病毒相互作用导致遗传抗性。一系列锁定产品 到目前为止鉴定的宿主因子，真核生物翻译起始因子4 E eIF（iso）4 E或其亚型eIF（iso）4 E作为eIF 4 E的遗传性病变是突出的 或eIF（iso）4 E可以赋予对许多病毒的免疫力， 特别是马铃薯Y病毒。不幸的是，潜在的机制仍然存在 难以捉摸。最近，我们发现eIF 4 E介导的耐药可能 与RNA靶向免疫相互关联。在这项研究中，我们还将 在病毒背景下从分子上理解和功能上表征eIF 4 E相互作用组 感染，特别是RNA靶向免疫在eIF 4 E介导的 利用遗传、分子和生物化学方法进行抗性研究。

Viral pathogens account for the largest proportion of newly emerging plant diseases and threaten global food security. To combat viruses, plants have evolved sophisticated defense mechanisms. In response, viruses have also evolved virulence strategies to counteract host defense. The long-term goal of our research program is to understand the complex virus-plant interactions, in particular the co-evolutionary arms race between viruses and plants, for the development of novel technologies to control viral diseases for sustainable crop production. An increasing body of evidence suggests that RNA-targeted immunity, which embraces RNA silencing, RNA decay and RNA quality control and regulates endogenous gene expression, is a central defense to viral pathogens in plants. These RNA immunity pathways may act in a hierarchical and concerted mode to inhibit virus infection with RNA silencing as a master player. RNA silencing, triggered by double-stranded RNA, is a fundamental, sequence-specific mechanism conserved in all eukaryotes. Viruses encode viral suppressors of RNA silencing (VSRs) that bind to cellular factors to cope with RNA silencing. Recently, we have found that VSRs also subvert RNA decay through interactions with key cellular decay pathway components to promote viral infection and autophagy plays contrasting roles (predominantly antiviral) in virus infection by regulating VSRs. As VSRs are highly diverse in sequence, they appear to interact with host proteins to execute their function. In this proposed research, we will identify host proteins that are recruited via interactions with VSRs to function specifically for RNA-targeted antiviral immunity rather than for endogenous gene regulation. We will further characterize their mechanistic details in the resistance-signaling pathway and elucidate how viruses interfere the antiviral function of these cellular factors using classical, molecular and cell biology techniques. Another emerging crucial antiviral defense is host factor-mediated recessive resistance. The vast majority of plant viruses have a small positive-sense, single-stranded RNA genome with very limited coding capacity. Thus, the invading virus depends on a number of host factors to establish its infection and disruption of the host factor-virus interaction leads to genetic resistance. Among a number of host factors identified so far, the eukaryotic translation initiation factor 4E (eIF4E) or its isoform eIF(iso)4E is outstanding as genetic lesions of eIF4E or eIF(iso)4E may confer immunity to a number of viruses, particularly potyviruses. Unfortunately, the underlying mechanism still remains elusive. Recently, we have found that eIF4E-mediated resistance may interlink with RNA-targeted immunity. In this proposed research, we will also molecularly understand and functionally characterize the eIF4E interactome in the context of virus infection, particularly the role of RNA-target immunity in eIF4E-mediated resistance using genetic, molecular and biochemical approaches.