A Bacterial Type III Effector Targets the Master Regulator of Salicylic Acid Signaling, NPR1, to Subvert Plant Immunity

Publication date: 13 December 2017
Source:Cell Host & Microbe, Volume 22, Issue 6
Author(s): Huan Chen, Jian Chen, Min Li, Ming Chang, Kaimei Xu, Zhenhua Shang, Yi Zhao, Ian Palmer, Yuqiang Zhang, Jon McGill, James R. Alfano, Marc T. Nishimura, Fengquan Liu, Zheng Qing Fu
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.

Graphical abstract

Teaser

NPR1, as the key transcriptional regulator of salicylic acid signaling, plays a pivotal role in plant local and systemic immunity. Chen et al. find that Pseudomonas syringae type III effector AvrPtoB directly targets the activated form of NPR1 for ubiquitination-mediated degradation to inhibit target gene expression, thereby dampening plant immunity.


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