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本文引用的文献

1
Bacterial effector HopF2 suppresses arabidopsis innate immunity at the plasma membrane.细菌效应因子 HopF2 在质膜处抑制拟南芥先天免疫。
Mol Plant Microbe Interact. 2011 May;24(5):585-93. doi: 10.1094/MPMI-07-10-0150.
2
Role of small RNAs in host-microbe interactions.小 RNA 在宿主-微生物相互作用中的作用。
Annu Rev Phytopathol. 2010;48:225-46. doi: 10.1146/annurev-phyto-073009-114457.
3
Different versions of Pseudomonas syringae pv. tomato DC3000 exist due to the activity of an effector transposon.不同版本的丁香假单胞菌 pv. 番茄 DC3000 因效应物转座子的活性而存在。
Mol Plant Pathol. 2006 Sep;7(5):355-64. doi: 10.1111/j.1364-3703.2006.00343.x.
4
Playing the "Harp": evolution of our understanding of hrp/hrc genes.演奏“竖琴”:我们对 hrc/hrp 基因理解的演变。
Annu Rev Phytopathol. 2010;48:347-70. doi: 10.1146/annurev-phyto-073009-114407.
5
The type III effector HopF2Pto targets Arabidopsis RIN4 protein to promote Pseudomonas syringae virulence.III 型效应因子 HopF2Pto 靶向拟南芥 RIN4 蛋白以促进丁香假单胞菌的毒性。
Proc Natl Acad Sci U S A. 2010 Feb 2;107(5):2349-54. doi: 10.1073/pnas.0904739107. Epub 2010 Jan 19.
6
Assay for pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) in plants.植物中病原体相关分子模式(PAMP)触发的免疫(PTI)检测
J Vis Exp. 2009 Sep 9(31):1442. doi: 10.3791/1442.
7
Recognitional specificity and evolution in the tomato-Cladosporium fulvum pathosystem.番茄-番茄叶霉病菌互作系统中的识别特异性与进化
Mol Plant Microbe Interact. 2009 Oct;22(10):1191-202. doi: 10.1094/MPMI-22-10-1191.
8
The majority of the type III effector inventory of Pseudomonas syringae pv. tomato DC3000 can suppress plant immunity.丁香假单胞菌番茄致病变种DC3000的大多数III型效应蛋白库能够抑制植物免疫。
Mol Plant Microbe Interact. 2009 Sep;22(9):1069-80. doi: 10.1094/MPMI-22-9-1069.
9
Recent advances in PAMP-triggered immunity against bacteria: pattern recognition receptors watch over and raise the alarm.病原体相关分子模式触发的抗细菌免疫的最新进展:模式识别受体进行监测并发出警报。
Plant Physiol. 2009 Aug;150(4):1638-47. doi: 10.1104/pp.109.139709. Epub 2009 Jun 26.
10
RNA silencing is required for Arabidopsis defence against Verticillium wilt disease.RNA沉默对于拟南芥抵御黄萎病是必需的。
J Exp Bot. 2009;60(2):591-602. doi: 10.1093/jxb/ern306. Epub 2008 Dec 19.

植物细菌 III 型效应因子 HopX1、HopAB1 和 HopF2 增强了 sense-后转录基因沉默,而不依赖于植物 R 基因-效应子识别。

Phytobacterial type III effectors HopX1, HopAB1 and HopF2 enhance sense-post-transcriptional gene silencing independently of plant R gene-effector recognition.

机构信息

Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology, Hellas, Crete, Greece.

出版信息

Mol Plant Microbe Interact. 2011 Aug;24(8):907-17. doi: 10.1094/MPMI-01-11-0010.

DOI:10.1094/MPMI-01-11-0010
PMID:21469938
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3788636/
Abstract

Plant- and animal-pathogenic bacteria deploy a variable arsenal of type III effector proteins (T3EP) to manipulate host defense. Specific biochemical functions and molecular or subcellular targets have been demonstrated or proposed for a growing number of T3EP but remain unknown for the majority of them. Here, we show that transient expression of genes coding certain bacterial T3EP (HopAB1, HopX1, and HopF2), which did not elicit hypersensitive response (HR) in transgenic green fluorescent protein (GFP) Nicotiana benthamiana 16C line, enhanced the sense post-transcriptional gene silencing (S-PTGS) triggered by agrodelivery of a GFP-expressing cassette and the silencing enhancement could be blocked by two well-known viral silencing suppressors. Further analysis using genetic truncations and site-directed mutations showed that the receptor recognition domains of HopAB1 and HopX1 are not involved in enhancing silencing. Our studies provide new evidence that phytobacterial pathogen T3EP manipulate the plant small interfering RNA pathways by enhancing silencing efficiency in the absence of effector-triggered immunity signaling and suggest that phytopathogenic bacterial effectors affect host RNA silencing in yet other ways than previously described.

摘要

植物和动物病原细菌利用可变的 III 型效应蛋白(T3EP)武器库来操纵宿主防御。越来越多的 T3EP 的特定生化功能和分子或亚细胞靶标已经得到证实或提出,但大多数 T3EP 的靶标仍然未知。在这里,我们表明,瞬时表达编码某些细菌 T3EP(HopAB1、HopX1 和 HopF2)的基因,这些基因在转绿色荧光蛋白(GFP)拟南芥 16C 系中不会引发过敏反应(HR),增强了由 GFP 表达盒农杆菌介导的感测转录后基因沉默(S-PTGS),而沉默增强可以被两种已知的病毒沉默抑制剂阻断。进一步的遗传截短和定点突变分析表明,HopAB1 和 HopX1 的受体识别结构域不参与增强沉默。我们的研究提供了新的证据,表明植物病原菌 T3EP 通过在没有效应触发免疫信号的情况下增强沉默效率来操纵植物小干扰 RNA 途径,并表明植物病原细菌效应物以以前未描述的其他方式影响宿主 RNA 沉默。