Autophagy is a ubiquitous intracellular degradation pathway, tightly controlled by more than 35 genes to secure cell homeostasis. This process acts at basal levels to maintain a continuous and effective intracellular clearance but it may also be induced in a number of stress conditions. Further, a selective process termed Mitophagy triggers the dismissal of damaged or useless mitochondria; it is strictly regulated by a number of specific factors, among which the mitochondria-ER contact sites. Comprehensively, autophagy and mitophagy control the struggle between cell death and survival during embryonic development and in adult organs, by cross-talking with cell cycle, cell motility, cell adhesion and cell secretion, and they help cells respond to external stimuli. As a consequence, these two processes are involved in the majority of human disorders, spanning from cancer to autoimmunity, from neurodegeneration to muscle dystrophy. Through this multidisciplinary project, we will address the outstanding
biological question of autophagy regulation and mitochondria homeostasis in neural and immune cellular differentiation, aiming at identifying novel druggable targets in human pathology.