Nuclear coat protein drives a multifaceted tolerance program during Turnip crinkle virus infection

Plant viruses must replicate yet maintain host tissue viability to sustain infection and transmission. We show that Turnip crinkle virus (TCV) uses nuclear localization of its coat protein (CP) to coordinate this balance. A nuclear-export mutant (TCVNES) retained core CP functions but causd attenuated symptoms and accumulated ~10-fold less than wild-type TCV. Transcriptomics and functional assays demonstrated that nuclear CP is required for large-scale host reprogramming, including SA accumulation and RBOH-dependent reactive oxygen species (ROS) production that promote TCV accumulation, as well as autophagy induction. Genetic loss of NADPH oxidase-derived ROS (rbohD rbohF) or autophagy (atg5-1) triggered rapid tissue collapse, necrosis, and convergent collapse-associated transcriptional responses following TCV infection. Nuclear CP consistently accelerated symptom onset in all backgrounds and exacerbated cell death and necrosis in rbohD rbohF and atg5-1. Nuclear CP is therefore responsible for early symptom development yet also required to activate ROS- and autophagy-dependent tolerance pathways.