Department of Plant Sciences, University of Cambridge, Cambridge, United Kingdom.
Adv Virus Res. 2010;76:57-121. doi: 10.1016/S0065-3527(10)76003-6. Epub 2010 Mar 31.
Induced mechanisms are by definition imperceptible or less active in uninfected, unstressed, or untreated plants, but can be activated by pathogen infection, stress, or chemical treatment to inhibit the replication and movement of virus in the host. In contrast, defenses that are pre-existing or serve to limit virus propagation and spread in otherwise susceptible hosts are considered to be "basal" in nature. Both forms of resistance can be genetically determined. Most recessive resistance genes that control resistance to viruses appear not to depend upon inducible mechanisms but rather maintain basal resistance by producing nonfunctional variants of factors, specifically translation initiation factors, required by the virus for successful exploitation of the host cell protein synthetic machinery. In contrast, most dominant resistance genes condition the induction of broad-scale changes in plant biochemistry and physiology that are activated and regulated by various signal transduction pathways, particularly those regulated by salicylic acid, jasmonic acid, and ethylene. These induced changes include localized plant cell death (associated with the hypersensitive response, HR) and the upregulation of resistance against many types of pathogen throughout the plant (systemic acquired resistance, SAR). Unfortunately, it is still poorly understood how virus infection is inhibited and restricted during the HR and in plants exhibiting SAR. Resistance to viruses is not always genetically predetermined and can be highly adaptive in nature. This is exemplified by resistance based on RNA silencing, which appears to play roles in both induced and basal resistance to viruses. To counter inducible resistance mechanisms, viruses have acquired counter-defense factors to subvert RNA silencing. Some of these factors may affect signal transduction pathways controlled by salicylic acid and jasmonic acid. In this chapter, we review current knowledge of defensive signaling in resistance to viruses including the nature and roles of low molecular weight, proteinaceous, and small RNA components of defensive signaling. We discuss the differences and similarities of defenses and defensive signaling directed against viral versus nonviral pathogens, the potential role of RNA silencing as an effector in resistance and possible regulator of defensive signaling, crosstalk and overlap between antiviral systems, and interference with and manipulation of host defensive systems by the viruses themselves.
诱导机制在未感染、未受胁迫或未经处理的植物中是不可察觉或活性较低的，但可以被病原体感染、胁迫或化学处理激活，从而抑制病毒在宿主中的复制和移动。相比之下，预先存在或旨在限制病毒在原本易感宿主中繁殖和传播的防御机制被认为是“基础”性质的。这两种形式的抗性都可以通过遗传决定。控制病毒抗性的大多数隐性抗性基因似乎不依赖于诱导机制，而是通过产生病毒成功利用宿主细胞蛋白合成机制所需的因素（特别是翻译起始因子）的无功能变体来维持基础抗性。相比之下，大多数显性抗性基因决定了植物生化和生理学的广泛变化的诱导，这些变化通过各种信号转导途径（特别是受水杨酸、茉莉酸和乙烯调节的途径）被激活和调节。这些诱导变化包括局部植物细胞死亡（与过敏反应 HR 相关）和整个植物中对多种类型病原体的抗性上调（系统获得性抗性 SAR）。不幸的是，人们仍然不太了解 HR 期间和表现出 SAR 的植物中病毒感染是如何被抑制和限制的。病毒抗性并不总是遗传上预先确定的，在性质上可以高度适应。这一点可以通过基于 RNA 沉默的抗性来说明，它似乎在病毒诱导和基础抗性中都发挥作用。为了对抗诱导性抗性机制，病毒已经获得了反防御因子来颠覆 RNA 沉默。其中一些因子可能会影响受水杨酸和茉莉酸控制的信号转导途径。在本章中，我们综述了抗病毒抗性中的防御信号转导的最新知识，包括防御信号转导中的低分子量、蛋白质和小 RNA 成分的性质和作用。我们讨论了针对病毒和非病毒病原体的防御和防御信号转导的差异和相似之处、RNA 沉默作为抗性的效应因子和防御信号转导的可能调节剂、抗病毒系统之间的串扰和重叠，以及病毒本身对宿主防御系统的干扰和操纵。
