TOR Inhibition Enhances Autophagic Flux and Immune Response in Tomato Plants Against PSTVd Infection

Abstract

Viroids are small, non-coding RNA pathogens known for their ability to cause severe plant diseases. Despite their simple structure, viroids like Potato Spindle Tuber Viroid (PSTVd) can interfere plant cellular processes, including both transcriptional and post-transcriptional mechanisms, thereby impacting plant growth and yield. In this study, we have investigated the role of the Target Of Rapamycin (TOR) signalling pathway in modulating viroid pathogenesis in tomato plants infected with PSTVd. Our findings reveal that PSTVd infection induces the accumulation of the selective autophagy receptor NBR1, potentially inhibiting autophagic flux. Pharmacological inhibition of TOR with AZD8055 mitigated PSTVd symptomatology by reducing viroid accumulation. Furthermore, TOR inhibition promoted the recovery of autophagic flux through NBR1 and primed the plant defence response, as evidenced by enhanced expression of both the defence-related gene PR1b and S5H, a gene involved in the salicylic acid catabolism. These results suggest a novel role for TOR in regulating viroid-induced pathogenesis and highlight the potential of TOR inhibitors as tools for enhancing plant resistance against viroid infections.