Uncovering Parallelophagy: How Viruses Trigger Multiple Autophagy Pathways

• Applicant: Dr. Marion Clavel, Ph.D.
• Subject Area: Organismic Interactions, Chemical Ecology and Microbiomes of Plant Systems ; Virology
• Term: since 2026
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 576847371

Viruses are ubiquitous parasites locked in a molecular arms race with their hosts. In plants, viral pathogens cause major agricultural losses and threaten food security and in animals, they can cause global pandemics. Viruses are master manipulators that hijack a broad range of processes and cause extensive cellular remodeling—offering a unique view into the cellular systems they reshape. Remarkably, plant viruses achieve this with a mere handful of proteins. One of the key cellular processes manipulated by viruses is selective autophagy—a precision cellular recycling mechanism that uses selective autophagy receptors (SARs) to recognize and eliminate unwanted cellular macromolecules. Although previous work showed that autophagy is induced during viral infection, which pathways are engaged or subverted—and their impact on infection or resistance—remains largely unknown. Unveiling these pathways is crucial to understand host-virus interactions and ultimately, the establishment and propagation of viral diseases. My lab has recently established that remodeling of the mitochondrial network by a single viral protein is sufficient to induce autophagy. Intriguingly, preliminary experiments also revealed that a dsRNA analog can independently trigger autophagy, suggesting that viruses may trigger distinct selective autophagy pathways in parallel. In this project we build on these observations and aim to dissect how plant viruses engage multiple selective autophagy pathways in parallel. We propose to generate a comprehensive map of selective autophagy pathways responding to a prototypic plant RNA virus. This will be pursued via a three-pronged approach: (1) Mapping of key viral components that underlie autophagy induction using quantitative cell biology assays developed in the host lab. (2) Discovery of selective autophagy pathways that are induced by viral infection, using autophagosome content-profiling proteomics. (3) A chemical perturbation screen mimicking viral infection for the elucidation of autophagy-inducing signals. Altogether, our findings will illuminate the molecular dialogue between viruses and autophagy and reveal novel molecular players involved in the virus-host arms race. As many viruses share infection strategies, we anticipate that our work could be harnessed to inform innovative antiviral strategies in plants and beyond.

• DFG Programme: Research Grants