Institute of Botany, University of Basel, Schönbeinstrasse 6, 4056 Basel, Switzerland.
Viruses. 2012 Oct 29;4(11):2578-97. doi: 10.3390/v4112578.
The frontline of plant defense against non-viral pathogens such as bacteria, fungi and oomycetes is provided by transmembrane pattern recognition receptors that detect conserved pathogen-associated molecular patterns (PAMPs), leading to pattern-triggered immunity (PTI). To counteract this innate defense, pathogens deploy effector proteins with a primary function to suppress PTI. In specific cases, plants have evolved intracellular resistance (R) proteins detecting isolate-specific pathogen effectors, leading to effector-triggered immunity (ETI), an amplified version of PTI, often associated with hypersensitive response (HR) and programmed cell death (PCD). In the case of plant viruses, no conserved PAMP was identified so far and the primary plant defense is thought to be based mainly on RNA silencing, an evolutionary conserved, sequence-specific mechanism that regulates gene expression and chromatin states and represses invasive nucleic acids such as transposons. Endogenous silencing pathways generate 21-24 nt small (s)RNAs, miRNAs and short interfering (si)RNAs, that repress genes post-transcriptionally and/or transcriptionally. Four distinct Dicer-like (DCL) proteins, which normally produce endogenous miRNAs and siRNAs, all contribute to the biogenesis of viral siRNAs in infected plants. Growing evidence indicates that RNA silencing also contributes to plant defense against non-viral pathogens. Conversely, PTI-based innate responses may contribute to antiviral defense. Intracellular R proteins of the same NB-LRR family are able to recognize both non-viral effectors and avirulence (Avr) proteins of RNA viruses, and, as a result, trigger HR and PCD in virus-resistant hosts. In some cases, viral Avr proteins also function as silencing suppressors. We hypothesize that RNA silencing and innate immunity (PTI and ETI) function in concert to fight plant viruses. Viruses counteract this dual defense by effectors that suppress both PTI-/ETI-based innate responses and RNA silencing to establish successful infection.
植物抵御非病毒病原体（如细菌、真菌和卵菌）的第一道防线是由跨膜模式识别受体提供的，这些受体可以检测到保守的病原体相关分子模式（PAMPs），从而引发模式触发免疫（PTI）。为了对抗这种先天防御，病原体部署了具有主要功能的效应蛋白来抑制 PTI。在特定情况下，植物进化出了能够检测到特定病原体效应蛋白的细胞内抗性（R）蛋白，从而引发效应触发免疫（ETI），这是 PTI 的放大版本，通常与过敏反应（HR）和程序性细胞死亡（PCD）相关。对于植物病毒，迄今为止尚未鉴定出保守的 PAMP，主要的植物防御被认为主要基于 RNA 沉默，这是一种进化保守的、序列特异性的机制，它调节基因表达和染色质状态，并抑制如转座子等侵入性核酸。内源性沉默途径产生 21-24 个核苷酸的小（s）RNA、miRNA 和短干扰（si）RNA，它们在后转录和/或转录水平上抑制基因表达。四种不同的 Dicer-like（DCL）蛋白通常产生内源性 miRNA 和 siRNA，它们都有助于感染植物中病毒 siRNA 的生物发生。越来越多的证据表明，RNA 沉默也有助于植物抵御非病毒病原体。相反，基于 PTI 的先天反应可能有助于抗病毒防御。同一 NB-LRR 家族的细胞内 R 蛋白能够识别非病毒效应蛋白和 RNA 病毒的无毒（Avr）蛋白，因此，在抗病毒宿主中触发 HR 和 PCD。在某些情况下，病毒 Avr 蛋白也作为沉默抑制子发挥作用。我们假设 RNA 沉默和先天免疫（PTI 和 ETI）协同作用来对抗植物病毒。病毒通过抑制基于 PTI/ETI 的先天反应和 RNA 沉默的效应子来对抗这种双重防御，从而建立成功的感染。
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