CHiC gene positively regulates the resistance to Botrytis cinerea in Arabidopsis

Membrane-localized GH18 chitinase CHiC boosts Arabidopsis resistance to Botrytis cinerea via SA/JA pathway activation, ROS suppression, and broad-spectrum immunity without growth penalty. Diseases are one of the major factors limiting the yield and quality of vegetables and other crops. Therefore, identifying and characterizing novel genes that enable plants to resist Botrytis cinerea (B. cinerea) infection, as well as elucidating their underlying mechanisms, are of significant theoretical importance and potential practical value. Chitinases are hydrolytic enzymes that break down chitin, a β-1,4-linked polymer of N-acetylglucosamine. Plant chitinases are central components of innate immunity, functioning in both pathogen recognition and pathogen restriction. The GH18 chitinase CHiC positively regulates Arabidopsis resistance to B. cinerea. CHiC expression is induced by pathogen infection and localized to the plasma membrane. Loss-of-function of CHiC increased susceptibility to B. cinerea and Pseudomonas syringae pv. tomato DC3000 (Pst. DC3000) with elevated ROS and malondialdehyde (MDA) levels. Conversely, overexpression lines exhibited reduced lesion size, pathogen biomass, and oxidative damage. CHiC activity peaked at 36 h post-inoculation, confirming enzymatic function in defense. Exogenous SA and JA induced CHiC expression. Under B. cinerea stress, CHiC activated SA pathway genes (PR1, PR2, PR5) and JA markers (PDF1.2a, ORA59), while mutants showed suppressed expression. This demonstrates CHiC's role in coordinating dual hormonal signaling for immunity. Critically, CHiC conferred broad-spectrum resistance without growth penalties. Our findings identify CHiC as a key immune regulator bridging chitinase activity, ROS homeostasis, and SA/JA pathways, providing a genetic resource for engineering disease-resistant crops.