丁香假单胞菌III型效应蛋白HopBB1促进宿主转录抑制因子降解以调控植物激素反应和毒力。
Pseudomonas syringae Type III Effector HopBB1 Promotes Host Transcriptional Repressor Degradation to Regulate Phytohormone Responses and Virulence.
作者信息
Yang Li, Teixeira Paulo José Pereira Lima, Biswas Surojit, Finkel Omri M, He Yijian, Salas-Gonzalez Isai, English Marie E, Epple Petra, Mieczkowski Piotr, Dangl Jeffery L
机构信息
Howard Hughes Medical Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Howard Hughes Medical Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
出版信息
Cell Host Microbe. 2017 Feb 8;21(2):156-168. doi: 10.1016/j.chom.2017.01.003. Epub 2017 Jan 26.
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 SCF 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.
来自生命三个分支（子囊菌、真细菌和卵菌）独立进化的病原体效应子汇聚到拟南芥TCP14转录因子上，以操纵宿主防御。然而，通过TCP14调控进行防御控制的机制基础尚不清楚。我们证明，TCP14通过转录抑制茉莉酸（JA）激素信号输出的一个子集来调节植物免疫系统。一种以前未被研究的丁香假单胞菌（Psy）III型效应子HopBB1与TCP14相互作用，并通过将其连接到JA信号阻遏物JAZ3，将其靶向SCF降解复合体。因此，HopBB1解除对JA反应基因中TCP14调控子集的抑制，并促进病原体毒力。因此，HopBB1通过精确操纵JA调控子的一部分来微调宿主植物激素信号转导，以避免多效性宿主反应，同时促进病原体增殖。
Zotero 插件