Bacterial pathogens and their hosts participate in a constantly evolving battle of attack, defence and counter-attack. In a paper recently published in Current Biology, researchers from Imperial College London and the University of the West of England show how one bacterial pathogen, through the power of evolution, achieves a significant advantage over its plant host. In this example, exposure of the invading microorganism to the defence mechanisms of the plant drives the evolution of a new virulent form of the pathogen through loss of a bacterial genomic island.

Bean pods naturally infected with halo-blight disease caused by Pseudomonas syringae pv. phaseolicola. Bacteria multiply in susceptible varieties, causing the characteristic water-soaked lesions shown here. In resistant varieties, they are restricted by the hypersensitive reaction. Image courtesy of J. Mansfield, Imperial College London UK.

Many phytopathogenic bacteria inject virulence effector proteins into plant cells through a type III secretion process. Without these effectors, the pathogens are unable to overcome basal host defences. However, some (termed avirulence) effectors can act as molecular double agents that betray the pathogen to plant defences. In these plants, resistance to infectious disease is based on the specific recognition of bacterial effectors by the products of resistance genes. When an effector is recognized, a hypersensitive resistance reaction (HR) is triggered that results in the establishment of a plant antimicrobial response. To investigate how bacterial pathogens overcome this form of host defence, Andrew Pitman and colleagues focused on the emergence of new virulent forms of Pseudomonas syringae pv. phaseolicola , the microorganism that is responsible for the economically important halo-blight disease of the common bean. This pathogen encodes a number of effectors that generate a hypersensitive resistance reaction when they encounter a plant with the corresponding resistance gene. When the authors repeatedly passaged the pathogen through bean leaves undergoing the resistant reaction, bacterial strains were selected that lacked the corresponding avirulence effector gene (avrPphB), which triggers the HR defence response in plants encoding the matching R3 resistance gene. After each passage, an increasing proportion of the bacterial colonies tested were able to cause disease, indicating a strong selective pressure to lose the effector gene. These experiments also gave the authors an unprecedented opportunity to directly observe the evolution of microbial pathogenicity in host tissue.

Further analysis of the deletion event revealed that avrPphB is part of a 106-kb genomic island (PPHGI-1) that shares strong similarities with integrative and conjugative elements and pathogenicity islands found in other bacteria — exposure of the pathogen to the HR resulted in deletion of the entire island. Surprisingly, the loss of this island did not seem to compromise the ability of the bacterium to grow and cause disease in the plant. The authors speculate that PPHGI-1, which contains genes encoding a type IV pilus and proteins involved in photosensory and chemotatic signalling, could confer a selective advantage to the bacterium under environmental conditions more relevant to its origins in the upland regions of East and Southern Africa.