The main interest of our group is to investigate autophagic mechanisms of protein homeostasis in neurons. Autophagy is an evolutionarily conserved process that delivers macromolecules and damaged or superfluous organelles to the lysosome for degradation. In addition, autophagic intermediates are also involved in non-degradative processes, participating in the unconventional secretion of proteins or their targeting to the plasma membrane. In line with these crucial functions, autophagy is indispensable for neuronal integrity and its deregulation causes severe synaptic defects that perturb behavior. However, the collective contribution of different autophagic processes to the homeostasis of synaptic proteins and to the function of neuronal subpopulations remain largely elusive.
Our work aims at characterizing the regulation and roles of degradative and secretory autophagy in the context of neuronal physiology and synaptic function. To this end, we use genetic mouse models, along with behavioral analyses and biochemical, cell biology and in vitro electrophysiology techniques. Moreover, we perform quantitative proteomic analyses in autophagic vesicles purified from the mouse brain.