Autophagy suppression by TORC1 maintains epithelial plasma membrane integrity and inhibits syncytium formation

Epithelial wound healing in Drosophila involves the formation of multinucleate cells surrounding the wound. We show that autophagy, a cellular degradation process often deployed in stress responses, is required for the formation of a multinucleated syncytium during wound healing. In addition, uncontrolled autophagy in the unwounded epidermis leads to the degradation of endo-membranes and the lateral plasma membrane, while the apical and basal membranes and the epithelial barrier function remain intact. Proper functioning of TORC1 is needed to prevent autophagy from destroying the larval epidermis, which depends on membrane isolation and phagophore expansion, but does not require the fusion of autophagosomes to lysosomes. Our findings reveal a function for TORC1-mediated regulation of autophagy in maintaining membrane integrity and homeostasis in the epidermis and during wound healing. Finally, autophagy can counteract experimentally induced nuclear defects resembling laminopathies. Key findings 1. A novel role for TORC1/autophagy pathway to control plasma membrane integrity and homeostasis. 2. Autophagy as the only known necessary and sufficient inducer of syncytium formation in the epithelium and during wound healing. ### Competing Interest Statement The authors have declared no competing interest.