BUI1 coordinates actin cytoskeleton remodeling and ROS homeostasis to confer broad-spectrum disease resistance in rice

The cytoskeleton functions as a dynamic intracellular structural scaffold, enabling cells to rapidly respond to biotic and abiotic stresses. During plant innate immunity, the cytoskeleton undergoes significant actin remodeling. Using the rice-Magnaporthe oryzae pathosystem, we demonstrate that pattern-triggered immunity (PTI) induces a rapid and transient actin filament reorganization dependent on the Class II formin protein BENT UPPERMOST INTERNODE1 (BUI1). Disruption of actin filaments using latrunculin B significantly enhances host susceptibility to the blast fungus M. oryzae. Importantly, the bui1 mutant exhibits compromised resistance not only to blast but also to the bacterial blight pathogen Xanthomonas oryzae pv. oryzae and the sheath blight fungus Rhizoctonia solani. We identify that this enhanced susceptibility to multiple pathogens stems from increased ROS scavenging activity in bui1, mediated by upregulation of peroxidase-encoding genes and consequent reduction in H₂O₂ accumulation. Furthermore, genetic analyses reveal that BUI1 acts downstream of the immunity suppressor RESISTANCE OF RICE TO DISEASES1 (ROD1), as the bui1 mutation compromises rod1-mediated broad-spectrum resistance. Our findings establish BUI1 as a key regulator linking cytoskeletal reorganization to receptor-mediated immune signaling and ROS homeostasis during plant-pathogen interactions, providing new insights into the integration of actin dynamics with plant defense mechanisms.