A fijivirus capsid protein hijacks autophagy degrading an ω-3 fatty acid desaturase to suppress jasmonate-mediated antiviral defence.

Plant viruses often suppress jasmonic acid (JA)-mediated defences through disturbing JA signalling or biosynthesis pathways to benefit their own infection. Few studies have examined how the precursors of JA biosynthesis are regulated by viral infection. In this study, we demonstrate that rice black-streaked dwarf virus (RBSDV) infection inhibits the production of α-linolenic acid (C18:3), a key JA biosynthesis precursor that is catalysed by a set of fatty acid desaturases (FADs). The viral capsid protein P10 directly interacts with OsFAD7, an ω-3 fatty acid desaturase, and promotes its autophagic degradation through an ATG8-interaction motif (AIM). This disrupts JA production and weakens antiviral defence against RBSDV infection. Genetic analysis reveals that overexpression of OsFAD7 enhances JA levels and resistance to virus. But OsFAD7-mediated antiviral resistance is attenuated if OsCOI1a, a JA receptor, is silenced, indicating that the enhancement of resistance to RBSDV infection conferred by OsFAD7 depends on the JA pathway. Our findings reveal a novel viral strategy that suppresses JA biosynthesis at its metabolic source, providing insights for developing viral protection strategies and virus-resistant crops.