Veinal necrosis induced by turnip mosaic virus infection in Arabidopsis is a form of defense response accompanying HR-like cell death.

In the pathosystems of Turnip mosaic virus (TuMV) with Brassicaceae crops, various symptoms, including mosaic and necrosis, are observed. We previously reported a necrosis-inducing factor TuNI in Arabidopsis thaliana, a model species. In this study, we show that the necrotic symptom induced by TuNI, observed along the veins, was actually a form of defense response accompanying a hypersensitive reaction (HR)-like cell death in the veinal area. The virus is often localized in the necrotic region. The necrotic response is associated with the production of H2O2, accumulation of salicylic acid (SA), emission of ethylene, and subsequent expression of defense-related genes. Additionally, this HR-like cell death is eased or erased by a shading treatment. These features are similar to the HR-associated resistance reaction to pathogens. However, unlike HR, two phytohormones--SA and ethylene--are involved in the necrosis induction, and both SA- and ethylene-dependent pathogenesis-related genes are activated. We concluded that the veinal necrosis induced by TuMV is regulated by a complex and unique network of at least two signaling pathways, which differs from the signal transduction for the known HR-associated resistance.