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

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

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 [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. ©2005 Elsevier Ltd All rights reserved.

• Journal Article Type: Article
• Publication Date: Dec 24, 2005
• Journal: Current Biology
• Print ISSN: 0960-9822
• Electronic ISSN: 1879-0445
• Publisher: Elsevier (Cell Press)
• Peer Reviewed: Peer Reviewed
• Volume: 15
• Issue: 24
• Pages: 2230-2235
• DOI: https://doi.org/10.1016/j.cub.2005.10.074
• Keywords: host resistance mechanisms, evolution, bacterial virulence, plants
• Public URL: https://uwe-repository.worktribe.com/output/1045757
• Publisher URL: http:dx.doi.org/10.1016/j.cub.2005.10.074
• Additional Information: Additional Information : Arnold was the Principal Investigator on this BBSRC-funded work and co-wrote the paper. She was group leader for the project and contributed to it experimentally by mutating the intergrase gene which led to the demonstration of its importance in the function of the pathogenicity island.