Arabidopsis Endoplasmic Reticulum-Localized UBAC2 Proteins Interact with PAMP-INDUCED COILED-COIL to Regulate Pathogen-Induced Callose Deposition and Plant Immunity
Arabidopsis Endoplasmic Reticulum-Localized UBAC2 Proteins Interact with PAMP-INDUCED COILED-COIL to Regulate Pathogen-Induced Callose Deposition and Plant Immunity
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DOI：
10.1105/tpc.18.00334
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发表时间：
2019-01
期刊：
影响因子：
11.6
通讯作者：
Zhe Wang;Xifeng Li;Xiaoting Wang;Nana Liu;Binjie Xu;Qi Peng;Zhifu Guo;B. Fan;Cheng Zhu;Zhixiang Chen
中科院分区：
文献类型：
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作者：
Zhe Wang;Xifeng Li;Xiaoting Wang;Nana Liu;Binjie Xu;Qi Peng;Zhifu Guo;B. Fan;Cheng Zhu;Zhixiang Chen
相互作用的ER蛋白UBAC 2和PICC积极调节PMR4胼胝质合成酶的积累，负责病原体诱导的胼胝质沉积在植物免疫反应。病原体相关分子模式（PAMP）触发的免疫（PTI）在PAMP被模式识别受体（PRR）识别后启动。PTI信号通过促分裂原活化蛋白激酶（MAPK）的活化传递，诱导信号传导和防御过程，例如活性氧（ROS）产生和胼胝质沉积。在这里，我们研究了两个拟南芥基因编码的同源物的泛素相关结构域含蛋白2（UBAC 2），一个保守的内质网（ER）蛋白质参与ER蛋白质的质量控制的突变体。ubac2突变体对细菌病原体假单胞菌的III型分泌缺陷型菌株过敏，表明PTI缺陷。ubac2突变体表现出正常的PRR生物发生、MAPK激活、ROS爆发和PTI相关基因表达。病原体和PAMP诱导的胼胝质沉积，然而，在ubac2突变体中受到损害。UBAC 2蛋白与植物特异性长卷曲螺旋蛋白PAMP诱导的卷曲螺旋（PICC）相互作用，并且picc突变体在胼胝质沉积和PTI中受到损害。受损的愈伤组织沉积在ubac2和picc突变体与减少积累的白粉病抗性4（PMR 4）的愈伤组织合成酶，这是负责病原体诱导的愈伤组织合成。组成性过表达PMR4恢复了ubac2和picc突变体中病原体诱导的胼胝质合成和PTI。这些结果揭示了一个ER途径，涉及保守的UBAC 2和植物特异性PICC蛋白，特异性调节病原体诱导的胼胝质沉积在植物先天免疫。
The interacting ER proteins UBAC2 and PICC positively regulate the accumulation of the PMR4 callose synthase responsible for pathogen-induced callose deposition during plant immune responses. Pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) is initiated upon PAMP recognition by pattern recognition receptors (PRR). PTI signals are transmitted through activation of mitogen-activated protein kinases (MAPKs), inducing signaling and defense processes such as reactive oxygen species (ROS) production and callose deposition. Here, we examine mutants for two Arabidopsis thaliana genes encoding homologs of UBIQUITIN-ASSOCIATED DOMAIN-CONTAINING PROTEIN 2 (UBAC2), a conserved endoplasmic reticulum (ER) protein implicated in ER protein quality control. The ubac2 mutants were hypersusceptible to a type III secretion-deficient strain of the bacterial pathogen Pseudomonas syringae, indicating a PTI defect. The ubac2 mutants showed normal PRR biogenesis, MAPK activation, ROS burst, and PTI-associated gene expression. Pathogen- and PAMP-induced callose deposition, however, was compromised in ubac2 mutants. UBAC2 proteins interact with the plant-specific long coiled-coil protein PAMP-INDUCED COILED COIL (PICC), and picc mutants were compromised in callose deposition and PTI. Compromised callose deposition in the ubac2 and picc mutants was associated with reduced accumulation of the POWDERY MILDEW RESISTANT 4 (PMR4) callose synthase, which is responsible for pathogen-induced callose synthesis. Constitutive overexpression of PMR4 restored pathogen-induced callose synthesis and PTI in the ubac2 and picc mutants. These results uncover an ER pathway involving the conserved UBAC2 and plant-specific PICC proteins that specifically regulate pathogen-induced callose deposition in plant innate immunity.