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 并被细菌 III 型效应子靶向

植物免疫受到复杂且动态的调控网络的严格控制，确保在检测到潜在病原体时得到最佳激活。因此，该网络的每个组成部分都是病原体操纵的潜在目标。在这里，我们报道了 RipAC，一种来自细菌病原体Ralstonia solanacearum的 III 型分泌效应子，以植物 E3 泛素连接酶 PUB4 为靶点，抑制模式触发免疫 (PTI)。PUB4 通过调节中枢免疫激酶 BIK1 的稳态在 PTI 中发挥积极作用。在PAMP感知之前，PUB4促进未激活的BIK1的降解，而在PAMP感知之后，PUB4有助于激活的BIK1的积累。RipAC 会导致 BIK1 降解，这与其 PTI 抑制活性相关。RipAC 会导致病原体相关分子模式 (PAMP) 诱导的 PUB4 积累和磷酸化减少。我们的结果阐明了 PUB4 在免疫调节中所发挥的作用，并说明了细菌效应子对免疫信号中枢 BIK1 的间接靶向。