The plant immune system is fundamental to plant survival in natural ecosystems and productivity in crop fields. Substantial evidence supports the prevailing notion that plants possess a two-tiered innate immune system, called pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). PTI is triggered by microbial patterns via cell surface-localized pattern-recognition receptors (PRRs), whereas ETI is activated by pathogen effector proteins via mostly intracellularly-localized receptors called nucleotide-binding, leucine-rich repeat proteins (NLRs)1-4. PTI and ETI are initiated by distinct activation mechanisms and are considered to have evolved sequentially5,6. Here we show that, contrary to the perception of PTI and ETI being separate immune signaling pathways, Arabidopsis PRR/co-receptor mutants, fls2/efr/cerk1 and bak1/bkk1/cerk1 triple mutants, are greatly impaired in ETI responses when challenged with incompatible Pseudomonas syrinage bacteria. We further show that the NADPH oxidase (RBOHD)-mediated production of reactive oxygen species (ROS) is a critical early signaling event connecting PRR and NLR cascades and that PRR-mediated phosphorylation of RBOHD is necessary for full activation of RBOHD during ETI. Furthermore, NLR signaling rapidly augments the transcript and protein levels of key PTI components at an early stage and in a salicylic acid-independent manner. Our study supports an alternative model in which PTI is in fact an indispensable component of ETI during bacterial infection, implying that ETI halts pathogen infection, in part, by directly co-opting the anti-pathogen mechanisms proposed for PTI. This alternative model conceptually unites two major immune signaling pathways in the plant kingdom and mechanistically explains the long-observed similarities in downstream defense outputs between PTI and ETI.

中文翻译：

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NLR介导的植物免疫力需要模式识别受体

植物免疫系统对于自然生态系统中的植物生存和农田的生产力至关重要。大量证据支持普遍的观点，即植物具有两级先天免疫系统，分别称为模式触发免疫（PTI）和效应触发免疫（ETI）。PTI由微生物模式通过细胞表面定位的模式识别受体（PRR）触发，而ETI由病原体效应蛋白通过大多数细胞内定位的受体（称为核苷酸结合，富含亮氨酸的重复蛋白（NLRs）1-4）激活。PTI和ETI由不同的激活机制引发，并被认为是依次发展的5,6。在这里，我们证明，与对PTI和ETI是独立的免疫信号通路的认识相反，拟南芥PRR / co-receptor突变体 当用不相容的假单胞菌syrinage细菌攻击时，fls2 / efr / cerk1和bak1 / bkk1 / cerk1三突变体在ETI反应中大大受损。我们进一步表明，NADPH氧化酶（RBOHD）介导的活性氧（ROS）的产生是连接PRR和NLR级联的关键早期信号传递事件，并且RBOHD的PRR介导的磷酸化对于ETI期间RBOHD的完全活化是必需的。此外，NLR信号在早期以水杨酸非依赖性的方式迅速增加了关键PTI组分的转录本和蛋白质水平。我们的研究支持一种替代模型，其中PTI实际上是细菌感染期间ETI必不可少的组成部分，这暗示ETI在某种程度上通过直接采用针对PTI提出的抗病原体机制来阻止病原体感染。