Pathogen small RNAs: a new class of effectors for pathogen attacks
Pathogen small RNAs: a new class of effectors for pathogen attacks
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DOI：
10.1111/mpp.12233
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发表时间：
2015-04-01
影响因子：
4.9
通讯作者：
Jin, Hailing
中科院分区：
文献类型：
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作者：
Wang, Ming;Weiberg, Arne;Jin, Hailing
近几十年来，植物病理学研究的深刻发现为我们理解病原体如何能够在活植物的生物生态位中定殖做出了巨大贡献。遗传学方法已经确定了致病性或毒力因素，对这些因素的探索拓宽了我们对宿主与病原体相互作用的理解。一组编码分泌蛋白的毒力基因被称为效应子，并且受到了广泛的关注，因为效应子会干扰和操纵宿主的感染防御途径。为了对抗病原体效应子，宿主植物进化出抗性（R）基因编码蛋白，与病原体效应子直接或间接相互作用，从而产生强烈的免疫反应，这一过程称为效应子触发免疫（ETI）。宿主和病原体之间发生进化军备竞赛，这驱使病原体重新发明其效应分子以破坏宿主植物的免疫力，并驱使宿主更新其分子免疫栅栏线以识别效应子并通过强化其免疫反应来击败病原体。 RNA 干扰 (RNAi) 或基因沉默是小 RNA (sRNA) 指导基因表达的转录和转录后沉默的机制。它是一种古老而保守的机制，存在于几乎所有真核生命形式中，包括植物、动物、真菌和卵菌。通常，sRNA 由 Dicer 样蛋白 (DCL) 产生，该蛋白将双链 RNA 或具有部分双链区域的单链 RNA 加工成成熟的 sRNA。成熟的 sRNA 被加载到 Argonaute (AGO) 蛋白中，并形成 RNA 诱导的沉默复合物 (RISC)。 RISC 沉默具有 sRNA 互补序列的基因。 RNAi 和 sRNA 在防御病毒和其他入侵 DNA 元件（例如转座子 (TE) 和转基因）方面发挥着重要作用。此外，sRNA在内源基因的表达调控中也发挥着重要作用。基因沉默发生在多种细胞过程中，包括植物针对各种病原体攻击的防御途径。植物内源sRNA在植物先天免疫中的调节作用已被深入研究。最近的证据还证明了病原体衍生的 sRNA 在宿主-微生物相互作用中的重要作用。在这里，我们主要讨论来自真核植物病原体的 sRNA 的作用，它们在感染过程中调节病原体或宿主内的基因表达。在这方面，病原体产生的 sRNA 可分为两类：（i）病原体内源 sRNA，在病原体细胞内感染期间调节重要的毒力基因（效应子）； (ii) sRNA 在感染过程中从病原体转移到宿主植物细胞中以沉默宿主免疫基因。这些病原体产生的 sRNA 可以指导宿主免疫基因的沉默，被称为 sRNA 效应子。病原体 sRNA 效应子导致的宿主基因沉默描述了宿主与病原体相互作用过程中跨界 RNAi 事件的新篇章。事实上，关于病原体和寄主植物之间的 RNA 和基于 RNAi 的通讯还有很多东西有待发现。
Over recent decades, profound findings in plant pathology research have made tremendous contributions to our understanding of how pathogens are able to colonize the biological niche of a living plant. Genetic approaches have determined pathogenicity or virulence factors, and the exploration of these factors has broadened our understanding of host–pathogen interactions. A group of virulence genes that code for secreted proteins are called effectors, and have received much attention, because effectors interfere with and manipulate host defence pathways for infection. To counter against pathogen effectors, host plants evolve resistance (R) gene-encoding proteins to interact directly or indirectly with pathogen effectors which mount a strong immune reaction, a process called effector-triggered immunity (ETI). An evolutionary arms race occurs between hosts and pathogens, which drives the pathogens to reinvent their effector molecules to undermine host plant immunity, and drives the hosts to update their molecular immune fence line to recognize effectors and to defeat pathogens by intensifying its immune response. RNA interference (RNAi) or gene silencing is a mechanism in which small RNAs (sRNAs) guide the transcriptional and posttranscriptional silencing of gene expression. It is an ancient and conserved mechanism present in almost all eukaryotic life forms, including plants, animals, fungi and oomycetes. Typically, sRNAs are generated by Dicer-like proteins (DCLs), which process double-stranded RNAs or single-stranded RNAs with partial double-stranded regions into mature sRNAs. The mature sRNAs are loaded into Argonaute (AGO) proteins, and form the RNA-induced silencing complex (RISC). The RISC silences genes with complementary sequences to sRNAs. RNAi and sRNAs are important players in defence against viruses and other invading DNA elements, such as transposons (TE) and transgenes. Moreover, sRNAs also play an important role in the regulation of the expression of endogenous genes. Gene silencing occurs in diverse cellular processes, including plant defence pathways against various pathogen attacks.The regulatory role of plant endogenous sRNAs in plant innate immunity has been studied intensively. Recent evidence has also demonstrated the important roles of pathogen-derived sRNAs in host–microbe interaction. Here, we mainly discuss the roles of sRNAs from eukaryotic plant pathogens, which regulate gene expression within pathogens or hosts during infection. In this regard, pathogen-produced sRNAs can be categorized into two groups:(i) pathogen endogenous sRNAs which regulate important virulence genes (effectors) during infection within pathogen cells; and (ii) sRNAs which translocate from the pathogens into the host plant cells during infection to silence host immunity genes. These pathogen-produced sRNAs, which direct the silencing of host immunity genes, are termed sRNA effectors. Host gene silencing by pathogen sRNA effectors describes a new chapter of crosskingdom RNAi events during host–pathogen interaction. Indeed, there is much more to be discovered about RNA and RNAi-based communication between pathogens and host plants.