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靠III型效应子引起疾病。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，但尚不清楚任何植物病原体效应物是否都靶向SA信号的主要调节因子NPR1。SA有助于将胞质NPR1寡聚体还原成单体，这些单体进入细胞核并充当植物防御基因的转录共激活因子。我们表明SA可以促进丁香假单胞菌之间的相互作用III型效应器AvrPtoB和NPR1。在SA的存在下，AvrPtoB以依赖于AvrPtoB的E3连接酶活性的方式通过宿主26S蛋白酶体介导NPR1的降解。有趣的是，我们发现NPR1在MAMP触发的免疫（MTI）中起重要作用，诱导MTI标记基因的表达。因此，这项工作揭示了一种策略，其中AvrPtoB靶向NPR1并抑制NPR1依赖性SA信号传导，从而破坏植物的先天免疫力。