Comparative genomics ofPseudomonas syringaereveals convergent gene gain and loss associated with specialisation onto cherry (Prunus avium)

Abstract

SummaryGenome-wide analyses of the effector- and toxin-encoding genes were used to examine the phylogenetics and evolution of pathogenicity amongst diverse strains ofPseudomonas syringaecausing bacterial canker of cherry (Prunus avium) including pathovarsP.spv.morsprunorum(Psm) races 1 and 2,P.spv.syringae(Pss) andP.spv.avii.Genome-based phylogenetic analyses revealedPsmraces andP.spv.aviiclades were distinct and were each monophyletic, whereas cherry-pathogenic strains ofPsswere interspersed amongst strains from other host species.A maximum likelihood approach was used to predict effectors associated with host specialisation on cherry.Psspossesses a smaller repertoire of type III effectors but has more toxin biosynthesis clusters compared withPsmandP.spv.avii. Evolution of cherry pathogenicity was correlated with gain of genes such ashopAR1andhopBB1through putative phage transfer and horizontal transfer, respectively. By contrast, loss of theavrPto/hopABredundant effector group was observed in cherry-pathogenic clades. Ectopic expression ofhopABandhopC1triggered the hypersensitive reaction in cherry leaves, confirming computational predictions.Cherry canker provides a fascinating example of convergent evolution of pathogenicity that is explained by the mix of effector and toxin repertoires acting on a common host.