背景回顾：Plant immunity is tightly controlled by a complex and dynamic regulatory network, which ensures optimal activation upon detection of potential pathogens. Accordingly, each component of this network is a potential target for manipulation by pathogens. 

主要发现：Here, we report that RipAC, a type III-secreted effector from the bacterial pathogen Ralstonia solanacearum, targets the plant E3 ubiquitin ligase PUB4 to inhibit pattern-triggered immunity (PTI). 

结果1-PUB4通过BIK1影响植物免疫：PUB4 plays a positive role in PTI by regulating the homeostasis of the central immune kinase BIK1. Before PAMP perception, PUB4 promotes the degradation of non-activated BIK1, while after PAMP perception, PUB4 contributes to the accumulation of activated BIK1. 

结果2-RipAC通过PUB4影响BIK1：RipAC leads to BIK1 degradation, which correlates with its PTI-inhibitory activity. RipAC causes a reduction in pathogen-associated molecular pattern (PAMP)-induced PUB4 accumulation and phosphorylation. 

结论：Our results shed light on the role played by PUB4 in immune regulation, and illustrate an indirect targeting of the immune signalling hub BIK1 by a bacterial effector.

植物免疫受到复杂且动态的调控网络的严格控制，从而保证在检测到潜在病原菌时最大化激发免疫。因此，该网络的每一个组分都是病原菌操纵的潜在靶标。本文中，作者报道了病菌性病原菌青枯雷尔氏菌分泌的III类效应子RipAC能够靶向植物E3泛素连接酶PUB4，从而抑制模式诱导免疫PTI。PUB4通过调控核心免疫激酶BIK1，在植物免疫PTI途径中扮演正向调控作用。在植物感知病原体相关分子模式（PAMP）之前，PUB4促进非激活态BIK1的降解，但是在感知PAMP之后，PUB4会作用于激活态BIK1的积累。RipAC会导致BIK1的降解，这与其抑制植物PTI的活性相关。RipAC会导致PAMP诱导的PUB4积累和磷酸化的减少。本文的研究结果揭示了PUB4在植物免疫中的调控作用，阐述了一个细菌效应子如何通过间接的方式靶向植物免疫信号转导的核心激酶BIK1。