A Bacterial Type III Effector Targets the Master Regulator of Salicylic Acid Signaling, NPR1, to Subvert Plant Immunity
A Bacterial Type III Effector Targets the Master Regulator of Salicylic Acid Signaling, NPR1, to Subvert Plant Immunity
复制标题
DOI：
10.1016/j.chom.2017.10.019
复制
发表时间：
2017-12-13
影响因子：
30.3
通讯作者：
Fu, Zheng Qing
中科院分区：
文献类型：
--
作者：
Chen, Huan;Chen, Jian;Fu, Zheng Qing
大多数植物细菌病原体依赖于III型效应子引起疾病。虽然众所周知，植物激素水杨酸（SA）在防御中起着至关重要的作用，但SA信号传导的主调节因子NPR 1是否被任何植物病原体效应物靶向尚不清楚。SA促进胞质NPR 1寡聚体还原成单体，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促进了假单胞菌III型效应AvrPtoB和NPR1之间的相互作用。在SA的存在下，AvrPtoB介导的降解NPR 1通过主机26 S蛋白酶体的方式依赖于AvrPtoB的E3连接酶活性。有趣的是，我们发现NPR 1在MAMP触发的免疫（MTI）中起着重要作用，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依赖的SA信号传导，从而颠覆植物先天免疫。
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.