Abstract/Summary

Pseudomonas syringae is a globally important plant pathogen, that includes pathovars that infect over 180 plant species. Individual pathovars are highly specialised and only infect one or a few hosts. Pseudomonas syringae uses a range of type III effector proteins to cause disease. However, plants have evolved to be able to detect these effectors and trigger immunity. Therefore, it is believed that a strain’s repertoire of effectors dictates its host range and genetic alteration of these repertoires enables host range expansion. This topic was explored using comparative genomics of three divergent clades that have convergently evolved to cause bacterial canker on cherry (Prunus avium). The clades include P. syringae pv. morsprunorum (Psm) (which is differentiated into two races based upon host response) and P. syringae pv. syringae (Pss). Three reference isolates of Psm R1, R2 and Pss were sequenced with PacBio and the genomes of a further fifteen isolates were sequenced using the Illumina MiSeq system. The virulence of strains was critically assessed in both lab- and field-based pathogenicity tests. Comparative genomic analysis of the Prunus strains revealed highly divergent effector and toxin repertoires within and between the different clades, indicating that they may each utilise distinct mechanisms to cause the same disease. Horizontal gene transfer of effector genes has occurred frequently between clades, often through the movement of plasmids. Several effectors, whose evolution is significantly associated with pathogenicity on Prunus were identified. Effectors that have been lost or putatively pseudogenised in cherry-infecting clades were cloned and expressed in pathogenic strains to determine if they are avirulence factors in cherry. The expression of two effectors (HopC1 and HopAB) was found to trigger a hypersensitive response on cherry leaves and reduce pathogen population growth. This work provides an insight into the convergent evolution of pathogenicity and mechanisms controlling the host specificity of bacteria.