Pseudomonas syringae is a highly diverse bacterial species complex that includes strains capable of infecting nearly all agronomically important crop species. However, individual P. syringae strains are highly host specific because of the complex evolutionary interplay between pathogen virulence factors and host immune systems. One critical virulence apparatus in P. syringae is the type III secretion system. This system is expected to play an important role in P. syringae host specificity because the type III secreted effectors that it deploys are collectively indispensable for virulence but can also activate host immunity. Using the pan-genome of nearly 500 strains isolated from more than 100 hosts, we characterized the distribution and diversity of effectors in the P. syringae species complex. We identified a total of 4,888 unique effector alleles and chemically synthesized 530 of these alleles to represent the breadth of diversity in effectors across all strains. By screening these representative alleles on the model host Arabidopsis thaliana, we find that nearly 10% of effectors elicit A. thaliana immunity and nearly all strains harbor at least one immune eliciting effector. These results suggest that effectors play a primary role in limiting the host range of P. syringae strains and likely explain why individual strains are so host specific. By linking recognizable effectors with the plant resistance genes that detect them, we can engineer more durably resistant crop cultivars that target the most vulnerable effectors in virulent P. syringae strains, ultimately limiting infectious disease outbreaks in critical crops.

I am an evolutionary geneticist working on the genomic determinants of host specificity in infectious diseases with Dr. David Guttman at the University of Toronto. My research combines bioinformatics, comparative genomics, experimental evolution, and functional screens to explore how pathogens respond to the challenges presented by new hosts and how they overcome these challenges to evolve new host specificities. I am also keenly interested in the mechanisms of mutation, as illustrated by my PhD work on the rates and biases of spontaneous mutations in bacteria with multiple chromosomes, which I completed at the University of New Hampshire. As I will soon be looking to obtain a tenure stream position in evolutionary genomics here in Canada, I am excited about the opportunity to contribute to this meeting and to forge collaborations with other researchers interested in the evolutionary genetics of infectious disease.