Journal
JOURNAL OF CELL BIOLOGY
Volume 181, Issue 7, Pages 1169-1177Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200712154
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Funding
- MRC [G0301172] Funding Source: UKRI
- Medical Research Council [G0301172] Funding Source: Medline
- Multiple Sclerosis Society [669] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
- Medical Research Council [G0301172] Funding Source: researchfish
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Rapid nerve impulse conduction in myelinated axons requires the concentration of voltage-gated sodium channels at nodes of Ranvier. Myelin-forming oligodendrocytes in the central nervous system (CNS) induce the clustering of sodium channels into nodal complexes flanked by paranodal axoglial junctions. However, the molecular mechanisms for nodal complex assembly in the CNS are unknown. Two isoforms of Neurofascin, neuronal Nfasc186 and glial Nfasc155, are components of the nodal and paranodal complexes, respectively. Neurofascin-null mice have disrupted nodal and paranodal complexes. We show that transgenic Nfasc186 can rescue the nodal complex when expressed in Nfasc(-/-) mice in the absence of the Nfasc 155-Caspr-Contactin adhesion complex. Reconstitution of the axoglial adhesion complex by expressing transgenic Nfasc155 in oligodendrocytes also rescues the nodal complex independently of Nfasc186. Furthermore, the Nfasc155 adhesion complex has an additional function in promoting the migration of myelinating processes along CNS axons. We propose that glial and neuronal Neurofascins have distinct functions in the assembly of the CNS node of Ranvier.
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