Robustness of plant quantitative disease resistance is provided by a decentralized immune network

International audience; Quantitative disease resistance (QDR) represents the predominant form of resistance in natural populations and crops. Surprisingly, very limited information exists on the biomolecular network of the signaling machineries underlying this form of plant immunity. This lack of information may result from its complex and quantitative nature. Here, we used an integrative approach including geno-mics, network reconstruction, and mutational analysis to identify and validate molecular networks that control QDR in Arabidopsis thaliana in response to the bacterial pathogen Xanthomonas cam-pestris. To tackle this challenge, we first performed a transcrip-tomic analysis focused on the early stages of infection and using transgenic lines deregulated for the expression of RKS1, a gene underlying a QTL conferring quantitative and broad-spectrum re-sistance to X. campestris. RKS1-dependent gene expression was shown to involve multiple cellular activities (signaling, transport, and metabolism processes), mainly distinct from effector-triggered immunity (ETI) and pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) responses already characterized in A. thaliana. Protein-protein interaction network reconstitution then revealed a highly interconnected and distributed RKS1-dependent network, organized in five gene modules. Finally, knockout mutants for 41 genes belonging to the different functional modules of the network revealed that 76% of the genes and all gene modules par-ticipate partially in RKS1-mediated resistance. However, these func-tional modules exhibit differential robustness to genetic mutations, indicating that, within the decentralized structure of the QDR net-work, some modules are more resilient than others. In conclusion, our work sheds light on the complexity of QDR and provides com-prehensive understanding of a QDR immune network.