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Keywords:

  • adult neurogenesis;
  • collective cell migration;
  • Rho family small GTPase

Abstract

Thumbnail image of graphical abstract

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.