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暴露于宿主抗性机制会推动植物中细菌毒力的进化。

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

作者信息

Pitman Andrew R, Jackson Robert W, Mansfield John W, Kaitell Victor, Thwaites Richard, Arnold Dawn L

机构信息

Centre for Research in Plant Science, University of the West of England, Bristol, BS16 1QY, United Kingdom.

出版信息

Curr Biol. 2005 Dec 20;15(24):2230-5. doi: 10.1016/j.cub.2005.10.074.

DOI:10.1016/j.cub.2005.10.074
PMID:16360685
Abstract

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 . In plants, varietal resistance to disease is based on recognition of effectors by the products of resistance (R) genes . When recognized, the effector or in this scenario, avirulence (Avr) protein triggers the hypersensitive resistance reaction (HR), which generates antimicrobial conditions . 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 . 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), 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 . We provide a molecular explanation of how exposure to resistance mechanisms in plants drives the evolution of new virulent forms of pathogens.

摘要

细菌对植物和动物的致病性是在攻击与防御的军备竞赛中进化而来的。关键因素是细菌效应蛋白,这些蛋白通过III型分泌系统传递并抑制基础防御。在植物中,品种对疾病的抗性基于抗性(R)基因产物对效应蛋白的识别。当被识别时,效应蛋白或在此情况下的无毒(Avr)蛋白会触发超敏抗性反应(HR),从而产生抗菌条件。不幸的是,这种基于基因对基因的抗性通常会失效,因为病原体的毒性菌株出现,不再触发HR。我们追踪了晕疫病病原体丁香假单胞菌菜豆致病变种在抗性菜豆品种叶片内新毒性致病型的出现。暴露于HR导致选择了缺乏无毒(效应)基因avrPphB(或hopAR1)的菌株,该基因在具有匹配R3抗性基因的品种中触发防御。avrPphB的缺失是通过删除一个106 kb的基因组岛(PPHGI - 1)实现的,该基因组岛与整合和接合元件(ICElands)以及不同细菌中的致病岛(PAIs)具有共同特征。我们提供了一个分子解释,说明植物中抗性机制的暴露如何驱动病原体新毒性形式的进化。

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