How the complex functionality of the nervous system arises from a pool of undifferentiated neuroepithelial cells during embryonic development is a fascinating process. We are investigating the role of autophagy in the development of the central nervous system in the mouse retina. Some autophagy deficient mice show developmental alterations that result in embryonic lethality. However, it remains unclear why autophagy is essential for proper development. We are investigating the relationship between autophagy and basic processes such as cell proliferation, differentiation, or death. Our data demonstrate that the metabolic activity of autophagy is essential to ensure proper neural differentiation in vivo and in vivo. Our research indicates that the autophagy pathways play multiple roles during embryonic development.

We have shown that selective mitochondrial degradation, a process known as mitophagy, regulates metabolic reprogramming during neurogenesis and mitophagy deficient animals display alterations in neuronal differentiation. In addition, this role of mitophagy in regulating the metabolism seems universal since it is also observed during the polarization of macrophages to a proinflammatory phenotype. We want to understand in precise molecular regulation of mitophagy and its links to metabolism under physiological and pathological conditions.