Pantoea ananatis-triggered systemic resistance requires root sensing through the LORE receptor kinase in Arabidopsis
Simon DuchateauiD, Jérôme CrouzetiD, Sylvain CordelieriD, Matthieu TouchardiD, Romain SchellenbergeriD, Célia Borrego, Sandra VillaumeiD, Jean-François GuiseiD, Qassim EsmaeeliD, Marie‐Christine GroleauiD, Maude CloutieriD, Charles GauthieriD, Sandrine Dhondt‐CordelieriD, Florence Mazeyrat‐GourbeyreiD, Fabienne BaillieuliD, Stefanie RanfiD, Éric DézieliD, Aziz AziziD, Stéphan DoreyiD
Abstract
Systemic immunity induced by beneficial bacteria helps plants to cope with subsequent pathogen attacks. However, how these bacteria are sensed by plants and how this sensing results in a systemic response is not well understood. Recently, the Brassicaceae LIPOOLIGOSACCHARIDE-SPECIFIC REDUCED ELICITATION (LORE) receptor kinase was identified as the direct sensor of bacterial medium-chain-length 3-hydroxy fatty acids (mc-3-OH-FAs) and 3-(3-hydroxyalkanoyloxy)alkanoic acids (HAAs), which activate systemic Brassicaceae immunity. Here, we show that the bacterium Pantoea ananatis BRT175, which produces HAAs, can colonize Arabidopsis thaliana roots independently of the production of these compounds. P. ananatis triggers induced systemic resistance (ISR) to the necrotrophic pathogen Botrytis cinerea, but not to the hemibiotrophic pathogen Pseudomonas syringae pv. tomato. Importantly, this ISR can be mimicked by HAAs or 3-hydroxy-decanoic acid (3-OH-C10). Both P. ananatis-triggered and 3-OH-C10-triggered ISR against B. cinerea are mediated by LORE sensing, involve salicylic acid, jasmonic acid and ethylene signaling pathways, and activate the expression of similar defense genes in infected leaves. Thus, 3-OH-C10 and HAAs are perceived by a pattern recognition receptor (PRR) in the root and activate a local immune response in roots as well as systemic immunity in leaves. Our study demonstrates that these lipidic microbe-associated molecular patterns (MAMPs), produced by beneficial microorganisms, are necessary and sufficient to trigger rhizobacteria-driven ISR. It further highlights the role of these MAMPs in differentially activating systemic resistance against biotrophic and necrotrophic pathogens.
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