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

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

Marion Clavel1,2,*, Anita Bianchi1, Roksolana Kobylinska1, Roan Groh1,3, Juncai Ma4, Ranjith K. Papareddy1, Nenad Grujic1, Lorenzo Picchianti1,3, Ethan Stewart5, Michael Schutzbier1, Karel Stejskal1, Juan Carlos de la Concepcion1, Victor Sanchez de Medina Hernandez1,3, Yoav Voichek1, Pieter Clauw1, Joanna Gunis1, Gerhard Durnberger1, Jens Christian Muelders2,  Annett Grimm2, Arthur Sedivy5, Mathieu Erhardt6, Victoria Vyboishchikov1, Peng Gao1, Esther Lechner6, Emilie Vantard6, Jakub Jez5, Elisabeth Roitinger1, Pascal Genschik6, Byung-Ho Kang4, Yasin Dagdas1,*

Affiliations

1Gregor Mendel Institute, Austrian Academy of Sciences, Vienna BioCenter, Vienna, Austria.

2Max-Planck-Institut für Molekulare Pflanzenphysiologie, Potsdam-Golm, Germany

3Vienna BioCenter PhD Program, Doctoral School of the University at Vienna and Medical University of Vienna, Vienna, Austria

4School of Life Sciences, Centre for Cell & Developmental Biology and State Key Laboratory of Agrobiotechnology, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, China

5Vienna Biocenter Core Facilities (VBCF), Vienna, Austria

6Institut de Biologie Moléculaire des Plantes, CNRS, Université de Strasbourg, 12, rue du Général Zimmer, 67084 Strasbourg, France

*Correspondence:           Marion Clavel ([e-mail]),

                                        Yasin Dagdas ([e-mail])

Abstract

RNA viruses co-opt the host endomembrane system and organelles to build replication complexes for infection. How the host responds to these membrane perturbations is poorly understood. Here, we explore the autophagic response of Arabidopsis thaliana to three viruses that hijack different cellular compartments. Autophagy is significantly induced within systemically infected tissues, its disruption rendering plants highly sensitive to infection. Contrary to being an antiviral defense mechanism as previously suggested, quantitative analyses of the viral loads established autophagy as a tolerance pathway. Further analysis of one of these viruses, the Turnip Crinkle Virus (TCV) that hijack mitochondria, showed that despite perturbing mitochondrial integrity, TCV does not trigger a typical mitophagy response.  Instead, TCV and Turnip yellow mosaic virus (TYMV) 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 such as EDS1. Altogether, our study reveals an autophagy-regulated metabolic rheostat that gauges cellular integrity during viral infection and degrades cell death executors to avoid catastrophic amplification of immune signaling.

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