The SCHENGEN pathway regulates lignin barrier formation via the receptor-like cytoplasmic kinase BIK1 in plant immunity

Abstract Lignin deposition is a hallmark of plant immunity, forming a physical barrier that restricts pathogen spread and confines hypersensitive cell death. However, how immune signaling triggers this barrier remains unclear. Here, we show that the Casparian strip surveillance pathway is repurposed during effector-triggered immunity to control lignin barrier formation. The peptide ligands CIF1 and CIF2 and their receptor SGN3 are transcriptionally induced upon avirulent bacterial infection and are required for pathogen-induced lignification and disease resistance. Mechanistically, SGN3 directly interacts with and phosphorylates BIK1, which acts as the primary downstream receptor-like cytoplasmic kinase in immune signaling. Genetic and molecular analyses further reveal that NLR-driven CIFs-SGN3-BIK1 signaling cooperates with pattern-recognition receptor pathways to promote ROS production and lignin polymerization during ETI. These findings uncover a previously unrecognized immune function of the SGN pathway and establish a signaling module linking pathogen recognition to lignin-based barrier formation.