A genomic island carrying a type III effector enters stealth mode in a pathogen population infecting a resistant plant.
Robert Jackson: University of Reading
<div>Bacterial pathogens evolve to overcome host resistance by different means. We have discovered that a <em>Pseudomonas syringae</em> pv. <em>phaseolicola</em> (<em>Pph</em>) bean pathogen carrying a genomic island encoding the type III effector <em>avrPphB</em> which triggers hypersensitive response (HR) immunity in a resistant bean plant, can evade the resistance response. This happens initially by the island excising from the chromosome to become a supercoiled episome that results in the downregulation of <em>avrPphB</em>. The pathogen then evolves over time by losing the genomic island from the cells – but this does not lead to island extinction because a sub-population (0.5% of the population) of cells with the island co-exist in a stealth mode with the dominant islandless population. We have developed a mathematical model to predict if the genomic island PPHGI-1 would be maintained in the population. We empirically tested the predictions made by the model and determined that PPHGI-1 frequency in the bacterial population drops during the HR. The island is then stably maintained in approximately 0.5% of the population over the long term. However, when a population of <em>Pph </em>that contains 0.5% cells carrying PPHGI-1 is inoculated into a bean cultivar that does not produce the HR, the proportion carrying PPGHI-1 increases rapidly suggesting that PPHGI-1 confers a fitness benefit. These results provide insights into the long term population dynamics of mobile genetic elements influencing pathogen evolution.</div>
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