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. 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). 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. 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. 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.

中文翻译：

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拟南芥E3泛素连接酶PUB4调节BIK1稳态并被细菌III型效应子靶向

植物免疫力由复杂而动态的调节网络严格控制，可确保在检测到潜在病原体时实现最佳激活。因此，该网络的每个组件都是病原体操纵的潜在目标。在这里，我们报道RipAC，从细菌病原体青枯菌（Ralstonia solanacearum）分泌III型效应子，靶向植物E3泛素连接酶PUB4以抑制模式触发的免疫（PTI）。PUB4通过调节中央免疫激酶BIK1的稳态来在PTI中发挥积极作用。在感知PAMP之前，PUB4促进未激活的BIK1的降解，而感知PAMP之后，PUB4导致激活的BIK1的积累。RipAC导致BIK1降解，这与其抑制PTI活性有关。RipAC导致减少病原体相关分子模式（PAMP）诱导的PUB4积累和磷酸化。我们的研究结果阐明了PUB4在免疫调节中的作用，并说明了细菌效应子对免疫信号中心BIK1的间接靶向。