Abstract
Newborn neurons migrate from their birthplace to their final location to form a properly functioning nervous system. During these movements, young neurons must attach and subsequently detach from their substrate to facilitate migration, but little is known about the mechanisms cells use to release their attachments. We show that the machinery for clathrin-mediated endocytosis is positioned to regulate the distribution of adhesion proteins in a subcellular region just proximal to the neuronal cell body. Inhibiting clathrin or dynamin function impedes the movement of migrating neurons both in vitro and in vivo. Inhibiting dynamin function in vitro shifts the distribution of adhesion proteins to the rear of the cell. These results suggest that endocytosis may play a critical role in regulating substrate detachment to enable cell body translocation in migrating neurons.
Highlights
IntroductionDisruptions in migration have been implicated in neurological disorders such as epilepsy, mental retardation, schizophrenia, and dyslexia [1,2,3]
Neuronal migration is critical for nervous system development
Components of clathrin-mediated endocytosis are enriched in the dilation of migrating neurons
Summary
Disruptions in migration have been implicated in neurological disorders such as epilepsy, mental retardation, schizophrenia, and dyslexia [1,2,3] Many of these disruptions are linked to cytoskeletal dysregulation, which impairs the directed motility of migrating neurons and prevents them from reaching their final destination. After the leading process extends but before the cell soma moves forward, a cytoplasmic dilation swells in the leading process proximal to the nucleus [5]. This dilation is characteristic of neurons migrating on many substrates from radial glia to extracellular matrix (ECM) [7,8,9,10].
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