ZmNPSN 13 Potentiates Maize Rough Dwarf Disease Upon Recruitment by the RBSDV P 7‐1 Effector

Maize rough dwarf disease (MRDD), caused by fijiviruses, poses a major threat to global maize production, with rice black-streaked dwarf virus (RBSDV) being the predominant pathogen in Asia. The viral effector P7-1 initiates MRDD by hijacking the host susceptibility factor ZmGDIα, while its reduced affinity for the helitron-inserted variant ZmGDIα-hel underlies recessive resistance. Here, we identified the Qb-SNARE protein ZmNPSN13 as a novel host target of P7-1. ZmNPSN13 functions as a central hub, interacting with both ZmGDIα and the gibberellin-inactivating enzyme ZmGA2ox7.3. During infection, P7-1 recruits these host components into a pathogenic complex that disrupts phytohormone homeostasis, thereby driving MRDD development. Notably, knockout of ZmNPSN13 restored hormonal balance and enhanced viral resistance comparable to that achieved by replacing ZmGDIα with ZmGDIα-hel. Our work uncovers a mechanism by which a virus exploits SNARE-mediated vesicle trafficking to subvert host immunity, establishing ZmNPSN13 as a promising target for engineering MRDD-resistant maize cultivars.