# Cytokinesis‐Defective 1 (CYT1) Positively Regulates Plant Antiviral Immunity by Promoting Callose Deposition and Ascorbic Acid Biosynthesis

## TL;DR

The study shows that the CYT1 protein helps plants fight viruses by boosting callose and ascorbic acid production, while the virus protein NIb interferes with these defenses.

## Contribution

This work identifies CYT1 as a novel regulator of plant antiviral immunity through callose and ascorbic acid pathways.

## Key findings

- CYT1 overexpression reduces TuMV infectivity in plants.
- CYT1 promotes callose deposition and ascorbic acid biosynthesis to enhance antiviral immunity.
- NIb interacts with CYT1 to inhibit its antiviral functions and promote viral infection.

## Abstract

NUCLEAR INCLUSION B (NIb), the RNA‐dependent RNA polymerase (RdRp) of potyviruses, plays a critical role in both viral replication and suppression of host antiviral immunity. However, the mechanisms by which NIb suppresses host immunity remain poorly understood. In this study, we used affinity purification‐mass spectrometry to identify host factors interacting with NIb encoded by turnip mosaic virus (TuMV). We identified 57 potential NIb‐interacting host factors, including mannose‐1‐phosphate guanylyltransferase CYTOKINESIS‐DEFECTIVE 1 (CYT1). Virus infectivity assays showed that TuMV infection was significantly attenuated in Nicotiana benthamiana leaves transiently expressing CYT1 and in transgenic Arabidopsis overexpressing CYT1. Exogenous application of ascorbic acid (AsA) and inhibition of N‐linked glycosylation reduced virus infection. Furthermore, overexpression of CYT1 induced callose deposition, and inhibition of callose synthesis enhanced virus infection. We also demonstrated that NIb interacts with the C‐terminal domain of CYT1, affects its cytosolic distribution, and inhibits AsA accumulation. These findings suggest that CYT1 positively regulates plant antiviral immunity by promoting callose deposition and ascorbic acid biosynthesis.

Turnip mosaic virus (TuMV)‐encoded NIb protein interacts with CYT1 to reduce callose deposition and ascorbic acid biosynthesis, while promoting N‐linked glycosylation to enable robust infection.