In a study published in Science, an international collaboration involving researchers from the IBMP sheds new light on the mechanisms that enable plants to cope with viral infections. The work reveals that selective autophagy, a cellular process responsible for the targeted recycling and removal of cellular components, plays a crucial role in limiting the damage caused by an excessive immune response.
By studying several RNA viruses infecting Arabidopsis thaliana, the researchers found that plants defective in autophagy developed much more severe symptoms and extensive necrosis. Surprisingly, this increased severity was not accompanied by higher levels of viral accumulation, suggesting that autophagy primarily protects the plant from the harmful consequences of its own defense responses rather than directly targeting the virus.
The study also uncovers an unexpected function for two families of metabolic enzymes, nitrilases (NIT) and inosine monophosphate dehydrogenases (IMPDH). During infection, these proteins contribute to the recruitment of immune regulators to the autophagy machinery. In particular, the researchers show that this mechanism controls the abundance of EDS1, a key regulator of plant immunity.
By limiting EDS1 accumulation, autophagy acts as a fine-tuning mechanism for immune responses and prevents the excessive activation of pathways leading to cell death. These findings reveal a new connection between cellular homeostasis, selective autophagy, and antiviral immunity, opening new perspectives for understanding how plants tolerate viral infections.
This study, coordinated by the teams of Marion Clavel and Yasin Dagdas, benefited from the contribution of researchers from the Institute of Plant Molecular Biology (IBMP, CNRS – University of Strasbourg): Mathieu Erhardt, Esther Lechner, Emilie Vantard, Thomas Potuschak and Pascal Genschik.
