Jackson, R. W. | Search bioRxiv

bioRxiv2018

Comparative genomics of Pseudomonas syringae reveals convergent gene gain and loss associated with specialisation onto cherry (Prunus avium)

O_LIGenome-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.\nC_LIO_LIGenome-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.\nC_LIO_LIA 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.\nC_LIO_LICherry 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.\nC_LI

microbiology↗

bioRxiv2017

Characterisation of the pathogenicity of strains of Pseudomonas syringae towards cherry and plum

Bacterial canker is a major disease of cherry and other stone fruits caused by several pathovars of Pseudomonas syringae. These are P.s pv. morsprunorum race 1 (Psm R1), P.s pv. morsprunorum race 2 (Psm R2) and P.s pv. syringae (Pss). Psm R1 and R2 were originally designated as races of the same pathovar, however phylogenetic analysis has revealed them to be distantly related. This study characterised the pathogenicity of P. syringae on cherry and plum, in the field and the laboratory. The field experiment identified variation in host cultivar susceptibility to the different pathogen clades. The cherry cultivar Merton Glory exhibited a broad resistance to all clades, whilst cultivar Van showed race-specific resistance. Psm R1 may be divided into a race structure with some strains pathogenic to both cherry and plum and others only pathogenic to plum. The results of laboratory-based pathogenicity tests were compared to results obtained on whole-trees. Only cut shoot inoculations were found to be sensitive enough to detect cultivar variation in susceptibility. Measuring population growth of bacteria in detached leaves reliably discriminated pathogens from non-pathogens. In addition, symptom appearance discriminated Psm races from non-pathogens which triggered a rapid hypersensitive response (HR). The pathogen Pss rapidly induced disease lesions and therefore may exhibit a more necrotrophic lifestyle than hemi-biotrophic Psm races. This in-depth study of pathogenic interactions, identification of host resistance and optimisation of laboratory assays, will provide a framework for future genetic dissection of virulence and host resistance mechanisms.

plant biology↗