Research Plant Cells: Cleanup Program Regulates Immune Response to Viral Infections

6 August 2026

Many of the most harmful viruses belong to the class of positive-sense single-stranded RNA viruses; these +ssRNA viruses also include deadly plant pathogens. Their genetic material consists of a single strand of RNA, which serves directly as a blueprint for the production of viral proteins. To create more copies of themselves, these viruses utilize the membranes inside the host cell, where they create optimal pockets for the production of additional viral copies. Prof. Dagdas and his team have studied the role of autophagy during a viral infection. Although it was previously known that the plant’s cleanup and recycling system – which acts as a “cleanup program” – plays a role in defending against viral infections, exactly how this occurs remained largely unclear.

The researchers first studied thale cress (Arabidopsis thaliana) plants in which autophagy was disrupted. They found that these plants were more susceptible to attacks by +ssRNA viruses. Unexpectedly, however, the cleanup program does not simply devour the viruses: Detailed analyses showed that plants with a disrupted cleanup and recycling system are not overrun by viruses or viral particles. Instead, autophagy responds to the damage that viruses cause inside the cells, as Dr. Marion Clavel explains. The scientist conducted research in Prof. Dagdas’ team and is currently a group leader at the Max Planck Institute for Molecular Plant Physiology in Potsdam.

When cells are attacked by viruses, cellular organelles such as the energy-producing mitochondria are restructured and severely deformed in the process. They develop membrane defects and change shape. This cellular stress triggers selective autophagy. In this process, only certain cellular components are recognized and forwarded as “cargo” for degradation. Prof. Dagdas and his team therefore set out to identify the receptors responsible for this process, which in this case specifically bind to the damaged mitochondria. To their surprise, the researchers discovered that two metabolic enzymes in the cell’s cytosol play a central role here.

Under normal conditions, the two enzymes, known as NIT1 and IMPDH, form long, filament-like structures. However, they break down into their individual units when, during a viral infection, the organelles rupture and their contents flow into the cytosol. In this altered state, the enzymes interact with both proteins that regulate cell death and the autophagy machinery. In this way, they ultimately direct the proteins that trigger cell death to be degraded. “By altering the balance between filaments and individual units, the plant can control how many of these proteins are degraded,” explains Prof. Dagdas, who heads the “Evolutionary Cell Biology” research group at the Centre for Organismal Studies at Heidelberg University.

The autophagy signaling pathway discovered by Prof. Dagdas and his team thus acts as a regulatory mechanism to control the extent of the immune response and establish a balance between defense and self-destruction. When a pathogen attacks, the cell must respond with an immune response, which, however, leads to cell death. If cells die too quickly during a viral infection, this causes systemic damage, resulting in the plant’s death. “Selective autophagy acts as a brake here and dampens an overactive immune response. It gives plant cells time to cope with the viral infection, thereby improving the plant’s chances of survival,” says Yasin Dagdas.

Researchers from the University of Strasbourg (France), the Vienna BioCenter Core Facilities (Austria), the Chinese University of Hong Kong, and the Max Planck Institute for Molecular Plant Physiology were also involved in the study. They received funding from, among others, the European Research Council and the Austrian Science Fund. The results of this research were published in “Science”.