The main focus of our research team is to understand how mammalian cells organelles and endomembranes cooperate with autophagic machinery to adapt to stress situations and external stimuli.
Most of mammalian intracellular compartments are highly regulated and renewed to ensure that complex trafficking and sorting functions occur properly and maintain normal cell physiology. In this dynamic context, the intracellular degradative autophagy pathway probably takes advantages of – and initiates dialogs with - pre-existing signaling platforms, organelles and endomembranes. Although there is low-level basal activity, autophagy is mostly associated with stress responses and is considered as an acute protective system that ensures cell homeostasis and contributes directly to cell metabolism and energy regulation. Accordingly, autophagy participates in development, immunity and protects against cell modifications related to ageing. Autophagy involves the formation, and subsequent trafficking, of autophagosomes, which arise from the closure of transient cup-shaped double-membrane structure termed phagophore that capture cytoplasmic cargos for a final delivery to lysosomes. Studying the crosstalk of autophagic machinery with other cellular organelles and structures, such as mitochondria, endosomes and primary cilia, will shed light on the importance of endomembranes and signaling platforms cooperation in stress sensing and homeostasis regulation in a wide variety of mammalian cells.
Our project aims at investigating the cellular and molecular mechanisms that regulate autophagic pathway during stress response in cooperation with other endomembranes, in physiological and pathophysiological situations.
More precisely, three interconnected axes are currently investigated in my laboratory: