Rac1-mediated indentation of resting neurons promotes the chain migration of new neurons in the rostral migratory stream of post-natal mouse brain
Article first published online: 25 NOV 2013
© 2013 International Society for Neurochemistry
Journal of Neurochemistry
Volume 128, Issue 6, pages 790–797, March 2014
How to Cite
J. Neurochem. (2014) 128, 790–797.
- Issue published online: 7 MAR 2014
- Article first published online: 25 NOV 2013
- Accepted manuscript online: 5 NOV 2013 07:28AM EST
- Manuscript Accepted: 30 OCT 2013
- Manuscript Revised: 18 SEP 2013
- Manuscript Received: 20 AUG 2013
- Japan Society for the Promotion of Science
- adult neurogenesis;
- collective cell migration;
- Rho family small GTPase
New neurons generated in the ventricular-subventricular zone in the post-natal brain travel toward the olfactory bulb by using a collective cell migration process called ‘chain migration.’ These new neurons show a saltatory movement of their soma, suggesting that each neuron cycles through periods of ‘rest’ during migration. Here, we investigated the role of the resting neurons in chain migration using post-natal mouse brain, and found that they undergo a dynamic morphological change, in which a deep indentation forms in the cell body. Inhibition of Rac1 activity resulted in less indentation of the new neurons in vivo. Live cell imaging using a Förster resonance energy transfer biosensor revealed that Rac1 was activated at the sites of contact between actively migrating and resting new neurons. On the cell surface of resting neurons, Rac1 activation coincided with the formation of the indentation. Furthermore, Rac1 knockdown prevented the indentation from forming and impaired migration along the resting neurons. These results suggest that Rac1 regulates a morphological change in the resting neurons, which allows them to serve as a migratory scaffold, and thereby non-cell-autonomously promotes chain migration.
New neurons generated in the ventricular-subventricular zone of the post-natal brain travel toward the olfactory bulb using a collective cell migration process called ‘chain migration.’ We found that chain-migrating neurons form an indentation in their cell body. Rac1 (Ras-related C3 botulinum toxin substrate 1) regulates the indentation in the resting neurons, which serve as a scaffold for the migrating neurons, thereby promoting chain migration non-cell-autonomously.