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

## TL;DR

This paper shows how a plant virus uses a protein in the cell nucleus to control infection and prevent host damage.

## Contribution

The study reveals a new role for viral coat protein in activating host tolerance mechanisms during infection.

## Key findings

- Nuclear localization of TCV coat protein is essential for host reprogramming and virus accumulation.
- Loss of ROS or autophagy leads to severe tissue damage and similar transcriptional responses.
- Nuclear CP both accelerates symptoms and prevents cell death through ROS and autophagy.

## Abstract

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.