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细菌效应因子 HopF2 在质膜处抑制拟南芥先天免疫。

Bacterial effector HopF2 suppresses arabidopsis innate immunity at the plasma membrane.

机构信息

Department of Plant Pathology and Microbiology, Texas A&M University, College Station, TX 77843, USA.

出版信息

Mol Plant Microbe Interact. 2011 May;24(5):585-93. doi: 10.1094/MPMI-07-10-0150.

DOI:10.1094/MPMI-07-10-0150
PMID:21198360
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3071429/
Abstract

Many bacterial pathogens inject a cocktail of effector proteins into host cells through type III secretion systems. These effectors act in concert to modulate host physiology and immune signaling, thereby promoting pathogenicity. In a search for additional Pseudomonas syringae effectors in suppressing plant innate immunity triggered by pathogen or microbe-associated molecular patterns (PAMPs or MAMPs), we identified P. syringae tomato DC3000 effector HopF2 as a potent suppressor of early immune-response gene transcription and mitogen-activated protein kinase (MAPK) signaling activated by multiple MAMPs, including bacterial flagellin, elongation factor Tu, peptidoglycan, lipopolysaccharide and HrpZ1 harpin, and fungal chitin. The conserved surface-exposed residues of HopF2 are essential for its MAMP suppression activity. HopF2 is targeted to the plant plasma membrane through a putative myristoylation site, and the membrane association appears to be required for its MAMP-suppression function. Expression of HopF2 in plants potently diminished the flagellin-induced phosphorylation of BIK1, a plasma membrane-associated cytoplasmic kinase that is rapidly phosphorylated within one minute upon flagellin perception. Thus, HopF2 likely intercepts MAMP signaling at the plasma membrane immediately of signal perception. Consistent with the potent suppression function of multiple MAMP signaling, expression of HopF2 in transgenic plants compromised plant nonhost immunity to bacteria P. syringae pv. Phaseolicola and plant immunity to the necrotrophic fungal pathogen Botrytis cinerea.

摘要

许多细菌病原体通过 III 型分泌系统将效应蛋白鸡尾酒注射到宿主细胞中。这些效应子协同作用,调节宿主的生理和免疫信号,从而促进致病性。在寻找抑制植物先天免疫的额外的丁香假单胞菌效应子方面,我们发现丁香假单胞菌番茄 DC3000 效应子 HopF2 是一种有效的早期免疫反应基因转录和由多种模式识别分子(PAMPs 或 MAMPs)激活的丝裂原活化蛋白激酶(MAPK)信号的抑制剂,包括细菌鞭毛蛋白、延伸因子 Tu、肽聚糖、脂多糖和 HrpZ1 harpin,以及真菌几丁质。HopF2 的保守表面暴露残基对于其 MAMP 抑制活性是必需的。HopF2 通过一个假定的豆蔻酰化位点靶向植物质膜,并且膜结合对于其 MAMP 抑制功能是必需的。HopF2 在植物中的表达强烈削弱了鞭毛蛋白诱导的 BIK1 的磷酸化,BIK1 是一种质膜相关的细胞质激酶,在感知鞭毛蛋白后一分钟内迅速磷酸化。因此,HopF2 可能在信号感知的质膜处立即拦截 MAMP 信号。与对多种 MAMP 信号的强烈抑制功能一致,HopF2 在转基因植物中的表达削弱了植物对细菌丁香假单胞菌 pv. Phaseolicola 的非宿主免疫和对坏死真菌病原体 Botrytis cinerea 的植物免疫。

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The long and winding road: virulence effector proteins of plant pathogenic bacteria.漫长而曲折的道路:植物病原菌的毒力效应蛋白。
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Bacterial virulence effectors and their activities.
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