Poster
Sabrina Gauthier
Universite de Sherbrooke
Sherbrooke, Quebec, Canada
Faye Gaudreault-Lafleur
Université de Sherbrooke
Sherbrooke, Quebec, Canada
Alexis Roy
Université de Sherbrooke
Sherbrooke, Quebec, Canada
Charles Roussin-Leveillee, PhD
Postdoc
University of Lausanne
Lausanne
Peter Moffett
Professor
Universite de Sherbrooke
Sherbrooke, Quebec, Canada
Effector-driven establishment of extracellular niche (EDEN) by pathogens in host plants is critical to a successful infection. Bacterial pathogens, such as Pseudomonas syringae pv. tomato DC3000, exploit this niche to colonize and proliferate within plant tissues by manipulating plant physiological processes to enrich the apoplast in water and nutritive metabolites. High atmospheric humidity levels provide ideal conditions for the formation of water-soaking lesions and thus, the creation of this favorable niche. In this context, we investigated the influence of apoplastic water levels on pathogen growth. We observed that maintaining an artificially flooded apoplast during infection enhances growth of both wild-type and effector mutant strains of Pst DC3000. Additionally, we observed that eliciting an ETI response induce the desiccation of plant tissues leading to microbial stasis. We also found that hydrating the apoplastic environment breaks microbial stasis induced by ETI. In parallel, artificial flooding prior to infection triggers plant immunity at levels comparable to flg22-induced protection, thereby reducing pathogenicity. These observations suggest that in addition to creating a favorable growth environment, pathogens induce an aqueous extracellular environment to suppress plant defenses. At the same time, given the ubiquity of water-soaking as a virulence strategy, we suggest that plants react to extracellular water in a manner similar to a DAMP/PAMP response.