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 of Pseudomonas syringae causing bacterial canker of cherry (Prunus avium) including pathovars P.s pv. morsprunorum (Psm) races 1 and 2, P.s pv. syringae (Pss) and P.s pv. avii.Genome-based phylogenetic analyses revealed Psm races and P.s pv. avii clades were distinct and were each monophyletic, whereas cherry-pathogenic strains of Pss were interspersed amongst strains from other host species.A maximum likelihood approach was used to predict effectors associated with host specialisation on cherry. Pss possesses a smaller repertoire of type III effectors but has more toxin biosynthesis clusters compared with Psm and P.s pv. avii. Evolution of cherry pathogenicity was correlated with gain of genes such as hopAR1 and hopBB1 through putative phage transfer and horizontal transfer, respectively. By contrast, loss of the avrPto/hopAB redundant effector group was observed in cherry-pathogenic clades. Ectopic expression of hopAB and hopC1 triggered 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.