Negative modulation of SA signaling components by the capsid protein of tobacco mosaic virus is required for viral long-distance movement

An important aspect of plant-virus interaction is the way viruses dynamically move over long distances and how plant immunity modulates viral systemic movement. Salicylic acid (SA), a well-characterized hormone responsible for immune responses against virus, is activated through different transcription factors including TGA and WRKY. In tobamoviruses, evidence suggests that capsid protein (CP) is required for long-distance movement, although its precise role has not been fully characterized yet. Previously, we showed that the CP of Tobacco Mosaic Virus (TMV)-Cg negatively modulates the SA-mediated defense. In this study, we analyzed the impact of SA-defense mechanism on the long-distance transport of a truncated version of TMV (TMV increment CP virus) that cannot move to systemic tissues. The study showed that the negative modulation of NPR1 and TGA10 factors allows the long-distance transport of TMV increment CP virus. Moreover, we observed that the stabilization of DELLA proteins promotes TMV increment CP systemic movement. We also characterized a group of genes, part of a network modulated by CP, involved in TMV increment CP long-distance transport. Altogether, our results indicate that CP-mediated downregulation of SA signaling pathway is required for the virus systemic movement, and this role of CP may be linked to its ability to stabilize DELLA proteins.

Automated summary

The study highlights the importance of the salicylic acid (SA) immune pathway in influencing the long-distance transport of Tobacco Mosaic Virus (TMV), through negative regulation of NPR1 and TGA10 factors. Furthermore, the stabilization of DELLA proteins by the capsid protein (CP) also plays a role in promoting the systemic movement of TMV.