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Characterization of a Natural Arabidopsis thaliana: Pseudomonas viridiflava Pathosystem


Duque Jaramillo,  A       
Department Molecular Biology, Max Planck Institute for Biology Tübingen, Max Planck Society;

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Duque Jaramillo, A. (2022). Characterization of a Natural Arabidopsis thaliana: Pseudomonas viridiflava Pathosystem. PhD Thesis, Eberhard-Karls-Universität, Tübingen, Germany.

Cite as: https://hdl.handle.net/21.11116/0000-000B-B600-7
Disease in plants can be caused by a variety of microorganisms, including bacteria. To fight infection, plants are equipped with an immune system that recognizes pathogens and activates a defense response mediated by the hormones salicylic acid and/or jasmonic acid and ethylene. One of the most important bacterial plant pathogens are strains from the Pseudomonas genus, able to infect crops and wild plants. The Pseudomonas syringae complex comprises most of the phytopathogens of this genus, including the model strain P. syringae pv. tomato DC3000 (DC3000), widely used in pathogenicity studies. P. viridiflava, a globally-distributed natural pathogen of the model plant Arabidopsis thaliana, also belongs to the P. syringae complex but is genetically and phenotypically distinct from well-characterized DC3000. Despite P. viridiflava being the most abundant Pseudomonas species in A. thaliana populations, little is known about the mechanisms of bacterial virulence and plant resistance in this pathosystem. In this thesis, I characterized the natural A. thaliana - P. viridiflava pathosystem by combining genetics, transcriptomics and metabolomics to identify resistance mechanisms in the host. I also used a computational framework to identify virulence-related specialized metabolites in the pathogen. In the first chapter, I investigated how P. viridiflava interacts with A. thaliana, and contrasted this with the model pathogen DC3000. I uncovered that the jasmonic acid/ethylene pathway is involved in defense against P. viridiflava, likely through an increase in jasmonic acid levels. Infection elicited a similar response in resistant and susceptible hosts, but the timing was different: changes occurred faster in the resistant host. In the second chapter, I explored how potential specialized metabolites encoded by P. viridiflava might be associated with differences in their virulence. I described the large biosynthetic potential of a collection of Pseudomonas genomes from the A. thaliana phyllosphere, and found that this biosynthetic potential is dominated by non-ribosomal peptide synthetases. I then identified gene cluster families with a putative role in P. viridiflava virulence, one of them related to the siderophore pyoverdine. Overall, this thesis presents an integrative approach to the study of plant-microbe interactions, and provides the baseline for further studies on the interactions between A. thaliana and P. viridiflava. This pathosystem better represents the interaction dynamics in natural populations and has the potential to address ecologically-relevant questions about adaptation and co-evolution of host and pathogen.