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Journal of Zhejiang University (Agriculture and Life Sciences)  2023, Vol. 49 Issue (5): 651-661    DOI: 10.3785/j.issn.1008-9209.2023.06.011
Special Topic: Major Bacterial and Viral Diseases in Crops     
Pathogenicity and avirulence mechanism of Ralstonia solanacearum type Ⅲ effectors
Peipei QI1,2,3(),Xiao YU1,2,3,Bo LI1,2,3()
1.National Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei 430070, China
2.The Provincial Key Lab of Plant Pathology of Hubei Province, College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, Hubei 430070, China
3.Hubei Hongshan Laboratory, Wuhan, Hubei 430070, China
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Abstract  

Ralstonia solanacearum is a very harmful plant pathogenic bacterium, and the plant bacterial wilt caused by it seriously affects the healthy production of tomato and potato crops. It has broad host varieties and can acquire new virulence through horizontal gene transfer and gene recombination to extend the host range. The pathogenic mechanism of R. solanacearum is complex, type Ⅲ secretion system (T3SS) is the key pathogenic factor, and the type Ⅲ effectors (T3Es) secreted by it play important roles in the pathogenic processand inhibit innate immune response of hosts at different levels. Moreover, plant hosts can recognize R. solanacearum effectors and activate effector-triggered immunity (ETI) to achieve disease resistance. In this review, the virulence and avirulence mechanisms of R. solanacearum T3Es were discussed and summarized, providing insights for further understanding the pathogenesis of R. solanacearum and the mechanisms of plant resistance to bacterial wilt.



Key wordsRalstonia solanacearum      bacterial wilt      effector      pathogenesis      innate immunity     
Received: 01 June 2023      Published: 25 October 2023
CLC:  S432.1  
Corresponding Authors: Bo LI     E-mail: 10152@mail.hzau.edu.cn;boli@mail.hzau.edu.cn
Cite this article:

Peipei QI,Xiao YU,Bo LI. Pathogenicity and avirulence mechanism of Ralstonia solanacearum type Ⅲ effectors. Journal of Zhejiang University (Agriculture and Life Sciences), 2023, 49(5): 651-661.

URL:

https://www.zjujournals.com/agr/10.3785/j.issn.1008-9209.2023.06.011     OR     https://www.zjujournals.com/agr/Y2023/V49/I5/651


青枯劳尔氏菌型效应子的致病和无毒机制

青枯劳尔氏菌(简称“青枯菌”)是一种危害十分严重的植物病原细菌,其引起的植物青枯病严重影响番茄和马铃薯等作物的健康生产。青枯菌寄主种类广泛,而且能够通过基因水平转移和基因重组获得新毒力,以扩展寄主范围。青枯菌的致病机制复杂,Ⅲ型分泌系统(type Ⅲ secretion system, T3SS)是关键的致病因子,其分泌的Ⅲ型效应子(type Ⅲ effectors, T3Es)在致病过程中发挥重要功能,从不同层面抑制寄主先天免疫反应;此外,植物寄主也能识别青枯菌的效应子,激活效应子触发的免疫反应并产生抗病性。本文对青枯菌Ⅲ型效应子的毒性机制与无毒功能进行了讨论和总结,为深入了解青枯菌的致病机制和植物抗青枯病的机制提供了思路。


关键词: 青枯劳尔氏菌,  细菌性青枯病,  效应子,  致病机制,  先天免疫 
Fig. 1 Schematic diagram of virulence functions of R. solanacearum T3EsBIK1: Botrytis-induced kinase 1; Ub: Ubiquitination; PUB4: Plant U-box protein 4; P: Phosphorylation; SGT1: Suppressor of the G2 allele of SKP1; MAPK: Mitogen-activated protein kinase; TRX: Thioredoxin; GSH: Glutathione; Ac: Acetylation; SA: Salicylic acid; JA: Jasmonic acid; TGA: TGACG motif binding protein; ADC: Arginine decarboxylase; PA: Polyamine; HR: Hypersensitive response; ROS: Reactive oxygen species; CATs: Catalases; JAZs: Jasmonate ZIM-domains; PDC: Pyruvate decarboxylase; TOR: Target of rapamycin; T6P: Trehalose-6-phosphate; CaM: Calmodulin; GAD: Glutamic acid decarboxylase; GABA: γ-aminobutyric acid; NAD+: Nicotinamide adenine dinucleotide; NADH: Reduced nicotinamide adenine dinucleotide.
Fig. 2 R. solanacearum T3Es recognized by different plants for triggering ETIA. Recognition of RipP2 by A. thaliana NLR protein complex RRS1-R/RPS4; B. Recognition of R. solanacearum T3Es by different Solanaceae plants (the plant icons in this figure are provided by https://www.biorender.com).
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