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Abstract:
The Pseudomonas syringae species complex comprises dozens of plant pathogenic strains with highly specific interactions with diverse host species and cultivars. My thesis research examines multiple stages of P. syringae’s coevolutionary interactions, from the earliest events involved in specialization to a novel host through to an assessment of the origin and evolution of the latest pandemic of this destructive infectious disease on Actinidia (kiwifruit) spp. The serial passaging of a strain of P. syringae on a novel host resulted in the appearance of an evolved line exhibiting higher growth on the novel host than the ancestor. The earliest steps towards host specialization were mutations in genes implicated in motility, exopolysaccharide production, and biofilm formation. The growth of this evolved line was compromised on its original host, suggesting there is a cost to specialization. The role of pathoadaptive variation as both a determinant of host specificity and the outcome of an arms race dynamic between P. syringae and its plant hosts was then investigated in order to develop a predictive method for the identification of novel innate immunity triggers. Plant hosts are more likely to evolve recognition to ‘core’ pathogen proteins under negative selection for the maintenance of essential functions, while repeated exposure to host defenses imposes strong selective pressure for elicitor diversification to avoid host recognition. Selected candidate elicitors were identified by screening a selection of plant pathogen genomes for these contrasting signatures of selection. Candidates were validated by testing their induction of Arabidopsis thaliana innate immunity. I conclude my thesis with an investigation into the origin and evolution of a recently emerged pandemic strain of P. syringae pv. actinidiae (Pan). Comparative genomic analyses of over 20 newly sequenced Pan strains revealed the outbreak strains form a distinct clade separate from Asian and Italian strains isolated prior to 2008. Outbreak-specific genes are frequently clustered together or with type 3 secreted effectors in mobile elements. Some outbreak-specific genes appear to have been acquired from vascular and woody pathogens, representing genes potentially involved in Pan’s ability to infect and spread through the woody tissues and vasculature of the kiwifruit vine.
