Abstract: Banded leaf and sheath blight (BLSB), incited by the necrotrophic basidiomycete Rhizoctonia solani, is a devastating soil-borne disease that severely constrains global maize (Zea mays) production. Bowman-Birk inhibitors (BBIs) constitute a critical class of protease inhibitors in plant innate immunity; yet, their biological functions and upstream regulatory circuits in maize defense against necrotrophic pathogens remain largely uncharacterized. Here, we show that ZmBBI1, a BBI family member transcriptionally upregulated upon R. solani infection, positively modulates BLSB resistance. Its defense activity is strictly dependent on trypsin-inhibitory function, mediated by the evolutionarily conserved Thr52 and Arg53 residues in its canonical reactive loop. We identify Rs03254, a secreted virulence effector from R. solani, that directly engages ZmBBI1 and biochemically inactivates its protease-inhibitory activity to promote fungal colonization. We further demonstrate that the conserved immune co-chaperone ZmSGT1 physically interacts with ZmBBI1 and is genetically required for its full defense function. Mechanistically, ZmSGT1 competes with Rs03254 for binding to ZmBBI1, displacing the pathogen effector and restoring ZmBBI1's trypsin-inhibitory activity. Our work defines a tripartite molecular arms race module in the maize-R. solani pathosystem and uncovers a noncanonical role for SGT1 as a molecular bodyguard that protects host defense factors from effector-mediated suppression, providing actionable targets for engineering durable BLSB resistance in maize.

Key words: fungal effector, maize, plant innate immunity, Rhizoctonia, solani, ZmBBI1, ZmSGT1