Abstract/Summary

Bacterial canker is a major disease of Prunus avium (cherry), Prunus domestica (plum) and other stone fruits. It is caused by pathovars within the Pseudomonas syringae species complex including P.s pv. morsprunorum race 1 (Psm R1), Psm R2 and P.s pv. syringae (Pss). Psm R1 and R2 were originally designated as the same pathovar, however phylogenetic analysis revealed them to be distantly related, falling into phylogroups 3 and 1 respectively. This study characterised the pathogenicity of 18 newly genome sequenced P. syringae strains on cherry and plum, in the field and laboratory. The field experiment confirmed that the cherry cultivar Merton Glory exhibited a broad resistance to all clades. Psm R1 contained strains with differential specificity on cherry and plum. The ability of tractable laboratory-based assays to reproduce assessments on whole trees was examined. Good correlations were achieved with cut shoot assays and leaves, although only the cut shoot assay was able to reliably discriminate cultivar differences seen in the field. Measuring bacterial multiplication in detached leaves differentiated pathogens from non-pathogens and was therefore suitable for routine testing. In cherry leaves, symptom appearance discriminated Psm races from non-pathogens which triggered a hypersensitive reaction. Pathogenic strains of Pss rapidly induced disease lesions in all tissues and exhibited a more necrotrophic lifestyle than hemibiotrophic Psm. This in-depth study of pathogenic interactions, identification of host resistance and optimisation of laboratory assays, provides a framework for future genetic dissection of host/pathogen interactions in the canker disease.