Why did filamentous plant pathogens evolve the potential to secrete hundreds of effectors to enable disease?
Why did filamentous plant pathogens evolve the potential to secrete hundreds of effectors to enable disease?
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DOI：
10.1111/mpp.12649
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发表时间：
2018-04
影响因子：
4.9
通讯作者：
H. Thordal-Christensen;P. Birch;P. Spanu;R. Panstruga
中科院分区：
文献类型：
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作者：
H. Thordal-Christensen;P. Birch;P. Spanu;R. Panstruga
在过去的十年中，许多基因组已从与植物进行生物营养相互作用的真菌和卵菌病原体中测序出来，即它们至少最初在活的植物组织上茁壮成长。这揭示了基因组通常编码数百种蛋白质，这些蛋白质预计是基于 N 端信号肽分泌的。这些蛋白质大多数是独特的或仅在有限的系统发育分支中发现（Franceschetti et al., 2017）。它们被预测为“效应子”，即以某种方式增强病原体毒力的蛋白质（见下文）。这些丝状微生物具有数百个候选效应基因，这一事实与细菌病原体形成鲜明对比，细菌病原体通常具有较少数量级的效应候选基因。尽管这数百个效应器中的大多数目前缺乏证据证明在毒力中发挥重要作用，但仍然令人惊讶的是，其中许多效应器似乎对毒力有可测量的贡献，并且其中一些效应器似乎与许多宿主蛋白发生物理相互作用。在这篇意见文章中，我们讨论了这些观察结果，并试图解决这些物种对数百个效应候选基因的明显需求。我们认为这一要求在一定程度上反映了效应器需要针对与防御无关的易感性成分。其中许多反过来可能会受到耐药性触发免疫传感器的监控（“防护”）。潜在地，病原体的成功取决于专门用于抑制这种监视的额外效应器组。植物免疫是复杂的，并被组织成所谓的“之字形模型”所描述的层（Jones 和 Dangl，2006）。植物利用病原体表现出不可或缺的病原体相关分子模式（PAMP）这一事实。这些分子通常被植物质膜驻留的模式识别受体（PRR）识别，从而激活模式触发免疫（PTI）。为了抑制 PTI，病原体会分泌效应物并将其传递给宿主。一些效应子被认为转移到宿主细胞质中，在那里它们可能被核苷酸结合的富含亮氨酸的重复型受体识别，也称为
During the past decade, many genomes have been sequenced from fungal and oomycete pathogens that interact biotrophically with plants, ie they thrive at least initially on living plant tissue. This has revealed genomes that often encode hundreds of proteins predicted to be secreted on the basis of N-terminal signal peptides. Most of these proteins are unique or found only within restricted phylogenetic clades (Franceschetti et al., 2017). They are predicted to be ‘effectors’, ie proteins which, in some way, contribute to the virulence of the pathogen (see below). The fact that these filamentous microbes have hundreds of candidate effector genes is in stark contrast with bacterial pathogens, which typically have an order of magnitude fewer effector candidate genes. Although most of these hundreds of effectors currently lack evidence for significant roles in virulence, it is still striking that many of them appear to contribute measurably to virulence and that several of them seem to physically interact with numerous host proteins. In this Opinion Piece, we discuss these observations and attempt to address the apparent need for hundreds of effector candidate genes in these species. We suggest that this requirement reflects, in part, the need for effectors to target defence-unrelated susceptibility components. Many of these, in turn, may be monitored (‘guarded’) by resistance-triggering immune sensors. Potentially, pathogen success depends on additional sets of effectors dedicated to suppress this kind of surveillance.Plant immunity is complex and organized into layers described by the so-called ‘zig–zag model’(Jones and Dangl, 2006). Plants exploit the fact that pathogens display indispensable pathogenassociated molecular patterns (PAMPs). These molecules are generally recognized by plant plasma membrane-resident pattern recognition receptors (PRRs), which activate pattern-triggered immunity (PTI). To suppress PTI, pathogens secrete and deliver effectors to the host. Some effectors are thought to be transferred to the host cytosol, where they may be recognized by nucleotidebinding leucine-rich repeat-type receptors, also referred to as