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Publication : Radial Glial Cell-Neuron Interaction Directs Axon Formation at the Opposite Side of the Neuron from the Contact Site.

First Author  Xu C Year  2015
Journal  J Neurosci Volume  35
Issue  43 Pages  14517-32
PubMed ID  26511243 Mgi Jnum  J:226681
Mgi Id  MGI:5698281 Doi  10.1523/JNEUROSCI.1266-15.2015
Citation  Xu C, et al. (2015) Radial Glial Cell-Neuron Interaction Directs Axon Formation at the Opposite Side of the Neuron from the Contact Site. J Neurosci 35(43):14517-32
abstractText  How extracellular cues direct axon-dendrite polarization in mouse developing neurons is not fully understood. Here, we report that the radial glial cell (RGC)-cortical neuron interaction directs axon formation at the opposite side of the neuron from the contact site. N-cadherin accumulates at the contact site between the RGC and cortical neuron. Inhibition of the N-cadherin-mediated adhesion decreases this oriented axon formation in vitro, and disrupts the axon-dendrite polarization in vivo. Furthermore, the RGC-neuron interaction induces the polarized distribution of active RhoA at the contacting neurite and active Rac1 at the opposite neurite. Inhibition of Rho-Rho-kinase signaling in a neuron impairs the oriented axon formation in vitro, and prevents axon-dendrite polarization in vivo. Collectively, these results suggest that the N-cadherin-mediated radial glia-neuron interaction determines the contacting neurite as the leading process for radial glia-guided neuronal migration and directs axon formation to the opposite side acting through the Rho family GTPases. SIGNIFICANCE STATEMENT: Neurons are highly polarized cell lines typically with a single axon and multiple dendrites, which underlies the ability of integrating and transmitting the information in the brain. How is the axon-dendrite polarity of neurons established in the developing neocortex? Here we show that the N-cadherin-mediated radial glial cell-neuron interaction directs axon-dendrite polarization, the radial glial cell-neuron interaction induces polarized distribution of active RhoA and active Rac1 in neurons, and Rho-Rho-kinase signaling is required for axon-dendrite polarization. Our work advances the overall understanding of how extracellular cues direct axon-dendrite polarization in mouse developing neurons.
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