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Simultaneous Interaction of Arabidopsis thaliana with Bradyrhizobium Sp. Strain ORS278 and Pseudomonas syringae pv. tomato DC3000 Leads to Complex Transcriptome Changes

¹Laboratoire des Symbioses Tropicales et Méditerranéennes (UMR113, Université Montpellier 2, Institut de Recherche pour le Développement, Cirad, Ecole Nationale Supérieure d'Agronomie de Montpellier, Institut National de la Recherche Agronomique), Université Montpellier 2, CC 002, Place Eugène Bataillon, 34095 Montpellier Cedex 5, France; ²Max Planck Institute of Molecular Plant Physiology, Am Muhlenberg 1, 14476 Golm, Germany; ³Unité de Recherche en Génomique Végétale (UMR 8114 Centre National de la Recherche Scientifique, Institut National de la Recherche Agronomique, Université d'Evry-Val d'Essonne), 2 rue Gaston Crémieux, CP5708-91057 Evry, France

Induced systemic resistance (ISR) is a process elicited by telluric microbes, referred to as plant growth-promoting rhizobacteria (PGPR), that protect the host plant against pathogen attacks. ISR has been defined from studies using Pseudomonas strains as the biocontrol agent. Here, we show for the first time that a photosynthetic Bradyrhizobium sp. strain, ORS278, also exhibits the ability to promote ISR in Arabidopsis thaliana, indicating that the ISR effect may be a widespread ability. To investigate the molecular bases of this response, we performed a transcriptome analysis designed to reveal the changes in gene expression induced by the PGPR, the pathogen alone, or by both. The results confirm the priming pattern of ISR described previously, meaning that a set of genes, of which the majority was predicted to be influenced by jasmonic acid or ethylene, was induced upon pathogen attack when plants were previously colonized by PGPR. The analysis and interpretation of transcriptome data revealed that 12-oxo-phytodienoic acid, an intermediate of the jasmonic acid biosynthesis pathway, is likely to be an actor in the signaling cascade involved in ISR. In addition, we show that the PGPR counterbalanced the pathogen-induced changes in expression of a series of genes.