Plant immunity is initiated by cell surface-localized receptors upon perception of pathogen-derived microbe or pathogen-associated molecular patterns (MAMPs/PAMPs), damage/danger-associated molecular patterns (DAMPs), and phytocytokines. Different patterns activate highly overlapping immune signaling at the early stage but divergent physiological responses at the late stage. Here, we indicate that plant elicitor peptide 1 (Pep1), a well-known DAMP, induces lignin and callose depositions, two types of late immune responses for strengthening the plant cell wall. Pep1-induced lignin and callose depositions in Arabidopsis root rely on early signaling components for Pep1 perception and signaling propagation. The phytohormone jasmonic acid and ethylene differently regulate the Pep1-regulated cell wall consolidation. Pep1 application in root also triggers a systemic immune signaling in shoot, and reactive oxygen species (ROS) is essential for the signaling communication between root and shoot. Collectively, the study reveals that Pep1 strengthens cell walls in root and triggers a systemic immune signaling from root to shoot.
Keywords: Arabidopsis; callose; jasmonic acid; lignin; plant elicitor peptide 1.