Abstract
In the course of their development from neuroepithelial cells to mature neurons, neuronal progenitors proliferate, delaminate, differentiate, migrate, and extend processes to form a complex neuronal network. In addition to supporting the morphology of the neuroepithelium and radial glia, polarity proteins contribute to the remodeling of processes and support the architectural reorganizations that result in axon extension and dendrite formation. While a good amount of evidence highlights a rheostat-like regulation by signaling events leading to local activation and/or redistribution of polarity proteins, recent studies demonstrate a new paradigm involving a switch-like regulation directly controlling the availability of polarity protein at specific stage by transcriptional regulation and/or targeted ubiquitin proteasome degradation. During the process of differentiation, most neurons will adopt a morphology with reduced polarity which suggests that polarity complex proteins are strongly repressed during key step of development. Here we review the different mechanisms that directly impact the levels of polarity complex proteins in neurons in relation to the polarization context and discuss why this transient loss of polarity is essential to understand neural development and how this knowledge could be relevant for some neuropathy.