TRR356 Seminar: Relieving the burden of replication: selective autophagy protects host cells against virus-induced organelle remodeling

Abstract:

RNA viruses are intracellular pathogen who depend on extensive manipulation of subcellular organelles to support their replication, significantly altering their morphology. Little is known about the cellular stress response involved in coping with such stress in both plants and animals. Selective autophagy is a well-established cellular quality control mechanism that is deployed to face a multitude of environmental and developmental challenges. Versatility and selectivity towards cargoes is achieved by a multitude of selective autophagy receptor (SAR) proteins, that bridge the interaction between cargo and ATG8. Using an AP-MS screen in ss(+)RNA viruses-Arabidopsis interactions, we identify two metabolic enzyme families that bind to ATG8 in an AIM-dependent manner and undergo virus-dependent autophagic degradation. We propose that these enzymes moonlight as SARs, as they transition to a monomeric state upon virus infection and enable autophagic degradation of pro-cell death factors. Thus, we uncover a critical function of selective autophagy in promoting survival in cells undergoing active viral replication and unproductive immune response.