Marion Clavel, A.T.J. Bianchi, Roksolana Kobylinska, Roan Groh, X Zhang, Juncai Ma, Ranjith K. Papareddy, Nenad Grujic, Lorenzo Picchianti, Ethan Stewart, Michael Schutzbier, Karel Stejskal, Juan Carlos De la Concepción, Víctor Sánchez de Medina Hernández, Yoav Voichek, Pieter Clauw, Joanna Gunis, Gerhard Dürnberger, Jens Christian Muelders, Annett Grimm, Arthur Sedivy, Mathieu Erhardt, Victoria Vyboishchikov, Peng Gao, Esther Lechner, Émilie Vantard, Thomas Potuschak, Jakub Jeż, Elisabeth Roitinger, Pascal Genschik, Byung-Ho Kang, Yasin Dagdas
RNA viruses co-opt host endomembranes to form replication complexes, often triggering cellular stress and immune responses. Here, we show that Arabidopsis thaliana activates selective autophagy to respond to viruses targeting mitochondria, chloroplasts, and the endoplasmic reticulum. Rather than degrading viral components, autophagy selectively removes the immune regulator Enhanced Disease Susceptibility 1 (EDS1) to prevent cell death. This targeted mechanism is mediated by oligomeric metabolic enzymes that moonlight as selective autophagy receptors, linking organelle stress to immune homeostasis. Our findings establish selective autophagy as an essential immune rheostat that fine-tunes defense responses and safeguards cellular integrity to promote host survival during viral infections.