Molecular Plant-Virus Interactions: Defense and Counter-defense

病毒病原体在新出现的疾病中所占比例最大 植物疾病，并威胁全球粮食安全。为了对抗病毒、植物 进化出复杂的防御机制。作为回应，病毒也 进化出的毒力策略来对抗宿主防御。的长期目标是 我们的研究计划是了解复杂的病毒-植物相互作用，在 特别是病毒和植物之间的共同进化军备竞赛，对于 开发控制病毒疾病的新技术以实现可持续发展 农作物生产。越来越多的证据表明，RNA靶向 免疫，包括RNA沉默、RNA衰变和RNA质量控制以及 调节内源性基因表达，是病毒病原体的中心防御 在植物中。这些RNA免疫途径可能以分层和协调的方式发挥作用 以RNA沉默为主的抑制病毒感染模式。核糖核酸 沉默，由双链RNA触发，是一种基本的， 序列特异性机制在所有真核生物中都是保守的。病毒编码病毒 与细胞因子结合以应对的RNA沉默抑制因子(VSR) RNA沉默。最近，我们发现VSR也通过 与关键的细胞衰变途径成分相互作用促进病毒 感染和自噬的作用截然不同(主要是抗病毒) 通过调节VSR来感染病毒。由于VSR在序列上高度多样化， 它们似乎与宿主蛋白相互作用来执行其功能。在这 在拟议的研究中，我们将确定通过 与VSR的相互作用对RNA靶向抗病毒起作用 免疫，而不是内源性的基因调节。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如何 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。另一个 新出现的关键的抗病毒防御是寄主因子介导的隐性抗性。 绝大多数植物病毒都有小的正链、单链 RNA基因组的编码能力非常有限。因此，入侵的病毒取决于 关于一些寄主因素确立其感染和破坏的 宿主因子与病毒的相互作用导致了遗传抗性。在众多的 宿主因子，真核翻译起始因子4E (EIF4E)或其亚型eIF(Iso)4E是突出的eIF4E遗传性病变 或者eIF(ISO)4E可以赋予对多种病毒的免疫力， 尤其是马铃薯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eIF4E介导的抗性可能 具有RNA靶向免疫的连锁。在这项拟议的研究中，我们还将 在病毒背景下对eIF4E相互作用组的分子理解和功能表征 感染，特别是RNA靶向免疫在eIF4E介导中的作用 利用遗传、分子和生物化学方法获得抗药性。

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.