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Abstract

During evolution of host-pathogen interactions, pathogens improve their virulence tools while hosts advance their defenses. Pseudomonas viridiflava, an opportunistic pathogen, is the most common Pseudomonas clade in European Arabidopsis thaliana populations. Belonging to the
P. syringae complex, it is genetically and phenotypically distinct from well-characterized P. syringae sensu stricto. Despite its broad range we lack knowledge of how A. thaliana responds to diverse co-occurring P. viridiflava strains and how they colonize A. thaliana. Here, we characterized the host response in a A. thaliana-P. viridiflava pathosystem. We measured host and pathogen growth in infections to ascertain gene × gene interactions and used immune mutants and transcriptomics to determine defense pathways influencing infection. We found a large effect of host genotype on infection outcome and evidence of host × pathogen genotype interaction. Immune mutant and transcriptome analyses
showed that A. thaliana uses jasmonic acid (JA)/ethylene (ET) signaling to defend itself against P. viridiflava, more so than salicylic acid. Our results suggest JA/ET is important for suppression of P. viridiflava, yet suppression capacity varies between accessions due to still unknown mechanisms. Our results shed light on how A. thaliana suppress the ever-present P. viridiflava, but further studies are needed to understand how this interaction contributes to persistence of P. viridiflava in A. thaliana populations.