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Myelination requires extensive plasma membrane rearrangements, implying that molecules controlling membrane dynamics play prominent roles. The large GTPase dynamin 2 (DNM2) is a well-known regulator of membrane remodeling, membrane fission, and vesicular trafficking. Here, we genetically ablated  Dnm2  in Schwann cells (SCs) and in oligodendrocytes of mice.  Dnm2  deletion in developing SCs resulted in severely impaired axonal sorting and myelination onset. Induced  Dnm2  deletion in adult SCs caused a rapidly-developing peripheral neuropathy with abundant demyelination. In both experimental settings, mutant SCs underwent prominent cell death, at least partially due to cytokinesis failure. Strikingly, when  Dnm2  was deleted in adult SCs, non-recombined SCs still expressing DNM2 were able to remyelinate fast and efficiently, accompanied by neuropathy remission. These findings reveal a remarkable self-healing capability of peripheral nerves that are affected by SC loss. In the central nervous system, however, we found no major defects upon  Dnm2  deletion in oligodendrocytes.

Schwann cells, but not Oligodendrocytes, Depend Strictly on Dynamin 2 Function