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Abstract

During evolution of host-pathogen interactions, pathogens improve their virulence tools while hosts advance their defenses. In wild populations, the genes underlying resistance and virulence are among the most polymorphic in the host and pathogen genomes respectively; however, it is not clear how this genetic diversity is maintained nor what its implications are for the evolution of host and pathogen. Pseudomonas viridiflava is the most common Pseudomonas clade in the phyllosphere of European Arabidopsis thaliana populations. It belongs to the P. syringae complex, but is genetically distinct from well-characterized P. syringae sensu stricto. P. viridiflava is genetically diverse and virulence varies among isolates. Furthermore, it has small repertoire of common virulence determinants such as effectors and toxins. Despite its broad distribution and prevalence, we lack knowledge of how A. thaliana responds to diverse co-occurring P. viridiflava strains and how they colonize and persist in the plant. During my PhD, I characterized the infection of A. thaliana by P. viridiflava. I measured host and pathogen growth to ascertain genotype x genotype interactions and used immune mutants, transcriptomics and metabolomics to determine defense pathways involved in infection response. I found a large effect of host genotype on infection outcome and evidence of host x pathogen genotype interactions. Immune mutant and transcriptome analyses showed that A. thaliana uses jasmonic acid (JA)/ethylene (ET) signaling to defend itself against P. viridiflava. Wounding of the plant increased resistance to infection, supporting the role of JA/ET in P. viridiflava suppression. However, suppression capacity varied between host genotypes due to still unknown mechanisms. Fine-scale genotype-by-genotype interactions may prevent a single bacterial strain from taking over in this natural pathosystem. Our results shed light on how A. thaliana fight off the ever-present pathogen P. viridiflava, but further studies are needed to understand the mechanisms of this interaction and how it contributes to persistence of P. viridiflava in A. thaliana populations.