Metabolic enzymes moonlight as selective autophagy receptors to protect plants against viral induced cellular damage

RNA viruses co-opt host intracellular structures to create specialized replication sites and advance infection. The response of the host to this membrane disruption is poorly understood. In this study, we explore Arabidopsis thaliana's reaction to three distinct viruses that commandeer varying cellular compartments. Our findings reveal autophagy is significantly induced within systemically infected tissues, with autophagy disruption rendering plants highly sensitive to infection. Contrary to being an antiviral defense, quantitative analyses of viral RNA and proteomes establish autophagy as a critical component of the host's tolerance mechanism. Further analysis of mitochondrial hijacking by the Turnip Crinkle Virus has shown that despite perturbing mitochondrial integrity, the virus does not trigger a typical mitophagy response. Instead, viral infection activates a distinct selective autophagy mechanism, where oligomeric metabolic enzymes moonlight as selective autophagy receptors and degrade key executors of defense and cell death. Altogether, our study reveals an autophagy-regulated metabolic rheostats that gauges cellular integrity during viral infection. For RNAseq analysis, the same samples as the ones used for TMT proteomics (PRIDE ID #PXD051596) were used to generate 3’TAG seq libraries