Plants suppress their immune system to survive viruses

Plants infected with positive-sense single-stranded RNA viruses trigger selective autophagy to limit damage caused by their own immune response. This mechanism does not reduce the amount of virus; it favors cell survival during systemic infection. This conclusion comes from a study with Arabidopsis thaliana.

Scientists evaluated three viruses. The turnip crinkle virus uses mitochondria. The turnip yellow mosaic virus uses chloroplasts. The turnip mosaic virus uses the endoplasmic reticulum. These viruses remodel organelles to form viral replication complexes. This process causes stress and interferes with cellular integrity.

Mutants with autophagy defects exhibited more severe symptoms and spontaneous necrosis. Even so, there was no detectable increase in the viral genome, viral proteins, or virion assembly. The result indicates a tolerance function, not direct resistance to the virus.

During infection associated with mitochondria, the formation of replication complexes coincided with mitochondrial clustering and membrane damage. Autophagy did not eliminate viral complexes or entire mitochondria. It removed mitochondrial matrix proteins released into the cytosol after membrane rupture.

The study identified two metabolic enzymes, nitrilase and inosine monophosphate dehydrogenase, as selective autophagy receptors. These proteins interacted with ATG8 and associated with the immune regulator EDS1. During infection, EDS1 underwent degradation via autophagy. The loss of EDS1 reduced necrosis in autophagy-deficient plants.

According to scientists at the Max Planck Institute, the process functions as a safety check for plant immunity. Instead of destroying the virus, the plant reduces part of the immune response to avoid tissue death. The researchers are now seeking to verify if this pathway occurs in other plant species or in infections caused by other pathogens.

Further information can be found at doi.org/10.1126/science.adu9554