一种细菌 III 型效应蛋白靶向水杨酸信号的主调控因子 NPR1，以颠覆植物的免疫。
A Bacterial Type III Effector Targets the Master Regulator of Salicylic Acid Signaling, NPR1, to Subvert Plant Immunity.
机构信息
Institute of Plant Protection, Jiangsu Academy of Agricultural Sciences, Nanjing, Jiangsu 210014, P. R. China; Department of Biological Sciences, University of South Carolina, Columbia, SC 29208, USA.
Department of Biological Sciences, University of South Carolina, Columbia, SC 29208, USA.
出版信息
Cell Host Microbe. 2017 Dec 13;22(6):777-788.e7. doi: 10.1016/j.chom.2017.10.019. Epub 2017 Nov 22.
Most plant bacterial pathogens rely on type III effectors to cause diseases. Although it is well known that the plant hormone salicylic acid (SA) plays an essential role in defense, whether the master regulator of SA signaling, NPR1, is targeted by any plant pathogen effectors is unknown. SA facilitates the reduction of cytosolic NPR1 oligomers into monomers, which enter the nucleus and function as transcriptional coactivators of plant defense genes. We show that SA promotes the interaction between the Pseudomonas syringae type III effector AvrPtoB and NPR1. In the presence of SA, AvrPtoB mediates the degradation of NPR1 via the host 26S proteasome in a manner dependent on AvrPtoB's E3 ligase activity. Intriguingly, we found that NPR1 plays an important role in MAMP-triggered immunity (MTI), inducing the expression of MTI marker genes. Thus, this work uncovers a strategy in which AvrPtoB targets NPR1 and represses NPR1-dependent SA signaling, thereby subverting plant innate immunity.
大多数植物细菌病原体依赖于 III 型效应物来引起疾病。尽管众所周知，植物激素水杨酸（SA）在防御中起着至关重要的作用，但植物防御基因的转录共激活因子 SA 信号的主要调节因子 NPR1 是否被任何植物病原体效应物靶向尚不清楚。SA 有助于将细胞质 NPR1 寡聚物还原为单体，这些单体进入细胞核并作为植物防御基因的转录共激活因子发挥作用。我们表明，SA 促进了丁香假单胞菌 III 型效应物 AvrPtoB 和 NPR1 之间的相互作用。在 SA 的存在下，AvrPtoB 通过宿主 26S 蛋白酶体介导 NPR1 的降解，这一过程依赖于 AvrPtoB 的 E3 连接酶活性。有趣的是，我们发现 NPR1 在 MAMP 触发的免疫（MTI）中发挥重要作用，诱导 MTI 标记基因的表达。因此，这项工作揭示了一种策略，即 AvrPtoB 靶向 NPR1 并抑制 NPR1 依赖的 SA 信号转导，从而颠覆植物先天免疫。
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