TY - JOUR
T1 - Radial glial cell–neuron interaction directs axon formation at the opposite side of the neuron from the contact site
AU - Xu, Chundi
AU - Funahashi, Yasuhiro
AU - Watanabe, Takashi
AU - Takano, Tetsuya
AU - Nakamuta, Shinichi
AU - Namba, Takashi
AU - Kaibuchi, Kozo
N1 - Publisher Copyright:
© 2015 the authors.
PY - 2015/10/28
Y1 - 2015/10/28
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84945535775&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84945535775&partnerID=8YFLogxK
U2 - 10.1523/JNEUROSCI.1266-15.2015
DO - 10.1523/JNEUROSCI.1266-15.2015
M3 - Article
C2 - 26511243
AN - SCOPUS:84945535775
VL - 35
SP - 14517
EP - 14532
JO - Journal of Neuroscience
JF - Journal of Neuroscience
SN - 0270-6474
IS - 43
ER -