Exposure to host resistance mechanisms drives evolution of bacterial virulence in plants

被引:96
作者
Pitman, AR
Jackson, RW
Mansfield, JW
Kaitell, V
Thwaites, R
Arnold, DL
机构
[1] Univ London Imperial Coll Sci Technol & Med, Div Biol, Ashford TN25 5AH, Kent, England
[2] Univ W England, Ctr Res Plant Sci, Bristol BS16 1QY, Avon, England
[3] Univ Bath, Dept Biol & Biochem, Bath BA2 7AY, Avon, England
[4] Cent Sci Lab, York YO41 1LZ, N Yorkshire, England
基金
英国生物技术与生命科学研究理事会;
关键词
D O I
10.1016/j.cub.2005.10.074
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Bacterial pathogenicity to plants and animals has evolved through an arms race of attack and defense. Key players are bacterial effector proteins, which are delivered through the type III secretion system and suppress basal defenses [1]. In plants, varietal resistance to disease is based on recognition of effectors by the products of resistance (R) genes [2]. When recognized, the effector or in this scenario, avirulence (Avr) protein triggers the hypersensitive resistance reaction (HR), which generates antimicrobial conditions [3]. Unfortunately, such gene-for-gene-based resistance commonly fails because of the emergence of virulent strains of the pathogen that no longer trigger the HR [4]. We have followed the emergence of a new virulent pathotype of the halo-blight pathogen Pseudomonas syringae pv. phaseolicola within leaves of a resistant variety of bean. Exposure to the HR led to the selection of strains lacking the avirulence (effector) gene avrPphB (or hopAR1 [5]), which triggers defense in varieties with the matching R3 resistance gene. Loss of avrPphB was through deletion of a 106 kb genomic island (PPHGI-1) that shares features with integrative and conjugative elements (ICElands) and also pathogenicity islands (PAIs) in diverse bacteria [6, 7]. We provide a molecular explanation of how exposure to resistance mechanisms in plants drives the evolution of new virulent forms of pathogens.
引用
收藏
页码:2230 / 2235
页数:6
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