期刊
JOURNAL OF NEUROSCIENCE
卷 35, 期 43, 页码 14517-14532出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1266-15.2015
关键词
axon formation; axon- dendrite polarization; cell-cell interaction; N-cadherin; radial glial cell; RhoA
资金
- MEXT KAKENHI [25123705, 221S0003]
- Japan Society for the Promotion of Science KAKENHI [25251021]
- Monbukagakusho (MEXT) Scholars
- Grants-in-Aid for Scientific Research [221S0003, 25251021] Funding Source: KAKEN
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.
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