The Chilli Veinal Mottle Virus Regulates Expression of the Tobacco Mosaic Virus Resistance Gene N and Jasmonic Acid/Ethylene Signaling Is Essential for Systemic Resistance Against Chilli Veinal Mottle Virus in Tobacco

Abstract

Genetic, physiological, and molecular analyses have revealed that the stress-related phytohormones salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) are known to participate in defense responses to mitigate biotic stress in plants. Recent evidence suggests that N-gene (a typical resistance gene) transcription is upregulated by Tobacco mosaic virus (TMV) infection, which is specifically a TMV-related phenomenon. In this study, we investigated N-gene transcription in tobaccoNN infected with Chilli veinal mottle virus (ChiVMV). Furthermore, we used a virus-induced gene-silencing-based genetics approach to investigate the function of SA, JA, and ET biosynthesis or signaling genes in systemic resistance to ChiVMV. Northern blot and qRT-PCR analysis indicate that N-gene transcription is stimulated by ChiVMV. Hormone measurements demonstrate that JA and ET increase rapidly during the early stages of ChiVMV infection, whereas SA increases slightly at later stages. JA and ET biosynthetic, signaling, and marker genes are significantly activated after ChiVMV inoculation, whereas SA biosynthetic, signaling, and marker genes are increased slightly. Silencing of JA, ET biosynthetic and signaling genes strongly increase the plants’ susceptibility to ChiVMV, whereas silencing of SA biosynthetic and signaling genes only partly compromise systemic resistance. Extensive ROS accumulate in JA, ET biosynthetic and signaling gene-silenced plants after ChiVMV infection, whereas only slight ROS produce in SA biosynthetic and signaling gene-silenced plants. Taken together, our results indicate that N-gene transcription is upregulated by ChiVMV infection, and the JA/ET pathways play an important role in plant systemic resistance against ChiVMV, whereas the SA pathway is only minorly involved.