Pseudomonas syringae Type III Effector HopBB1 Promotes Host Transcriptional Repressor Degradation to Regulate Phytohormone Responses and Virulence.
Pseudomonas syringae Type III Effector HopBB1 Promotes Host Transcriptional Repressor Degradation to Regulate Phytohormone Responses and Virulence.
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DOI：
10.1016/j.chom.2017.01.003
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发表时间：
2017-02-08
影响因子：
30.3
通讯作者：
Dangl JL
中科院分区：
文献类型：
--
作者：
Yang L;Teixeira PJ;Biswas S;Finkel OM;He Y;Salas-Gonzalez I;English ME;Epple P;Mieczkowski P;Dangl JL
来自三个生命分支（子囊菌、真细菌和卵菌）的独立进化的病原体效应子会聚到拟南芥TCP14转录因子上以操纵宿主防御。然而，通过TCP14调节进行防御控制的机制基础是未知的。我们证明，TCP14调节植物免疫系统的转录抑制茉莉酸（JA）激素信号输出的一个子集。以前未研究的假单胞菌（Psy）III型效应子HopBB1与TCP 14相互作用，并通过将其连接到JA信号抑制子JAZ3将其靶向SCFCOI1降解复合物。因此，HopBB1去抑制TCP14调节的JA应答基因子集，并促进病原体毒力。因此，HopBB1通过精确操纵JA调节子的一部分来微调宿主植物激素串扰，以避免多效性宿主反应，同时促进病原体增殖。Yang等人证明，假单胞菌III型效应子HopBB1调节植物茉莉酸（JA）信号传导的两个负调节因子TCP14和JAZ3，并将它们“粘合”在一起进行降解，从而精确激活促进细菌毒力的JA输出反应的子集。
Independently evolved pathogen effectors from three branches of life (ascomycete, eubacteria and oomycete) converge onto the Arabidopsis TCP14 transcription factor to manipulate host defense. However, the mechanistic basis for defense control via TCP14 regulation is unknown. We demonstrate that TCP14 regulates the plant immune system by transcriptionally repressing a subset of the Jasmonic acid (JA) hormone signaling outputs. A previously unstudied Pseudomonas syringae (Psy) type III effector, HopBB1, interacts with TCP14 and targets it to the SCFCOI1- degradation complex by connecting it to the JA signaling repressor JAZ3. Consequently, HopBB1 de-represses the TCP14-regulated subset of JA response genes and promotes pathogen virulence. Thus, HopBB1 fine-tunes host phytohormone crosstalk by precisely manipulating part of the JA regulon to avoid pleiotropic host responses, while promoting pathogen proliferation. Yang et al. demonstrate that the Pseudomonas syringae type III effector HopBB1 modulates two negative regulators of plant Jasmonic acid (JA) signaling, TCP14 and JAZ3, and ‘glues’ them together for degradation, resulting in precise activation of a subset of JA output responses that promote bacterial virulence.