Accumulation of Neurofascin at Nodes of Ranvier Is Regulated by a Paranodal Switch.
Schwann cell
myelin
neurofascin
node of Ranvier
oligodendrocyte
paranodes
Journal
The Journal of neuroscience : the official journal of the Society for Neuroscience
ISSN: 1529-2401
Titre abrégé: J Neurosci
Pays: United States
ID NLM: 8102140
Informations de publication
Date de publication:
22 07 2020
22 07 2020
Historique:
received:
10
04
2019
revised:
29
04
2020
accepted:
02
06
2020
pubmed:
20
6
2020
medline:
29
12
2020
entrez:
20
6
2020
Statut:
ppublish
Résumé
The paranodal junctions flank mature nodes of Ranvier and provide a barrier between ion channels at the nodes and juxtaparanodes. These junctions also promote node assembly and maintenance by mechanisms that are poorly understood. Here, we examine their role in the accumulation of NF186, a key adhesion molecule of PNS and CNS nodes. We previously showed that NF186 is initially targeted/accumulates via its ectodomain to forming PNS (hemi)nodes by diffusion trapping, whereas it is later targeted to mature nodes by a transport-dependent mechanism mediated by its cytoplasmic segment. To address the role of the paranodes in this switch, we compared accumulation of NF186 ectodomain and cytoplasmic domain constructs in WT versus paranode defective (i.e., Caspr-null) mice. Both pathways are affected in the paranodal mutants. In the PNS of Caspr-null mice, diffusion trapping mediated by the NF186 ectodomain aberrantly persists into adulthood, whereas the cytoplasmic domain/transport-dependent targeting is impaired. In contrast, accumulation of NF186 at CNS nodes does not undergo a switch; it is predominantly targeted to both forming and mature CNS nodes via its cytoplasmic domain and requires intact paranodes. Fluorescence recovery after photobleaching analysis indicates that the paranodes provide a membrane diffusion barrier that normally precludes diffusion of NF186 to nodes. Linkage of paranodal proteins to the underlying cytoskeleton likely contributes to this diffusion barrier based on 4.1B and βII spectrin expression in Caspr-null mice. Together, these results implicate the paranodes as membrane diffusion barriers that regulate targeting to nodes and highlight differences in the assembly of PNS and CNS nodes.
Identifiants
pubmed: 32554548
pii: JNEUROSCI.0830-19.2020
doi: 10.1523/JNEUROSCI.0830-19.2020
pmc: PMC7380970
doi:
Substances chimiques
Cell Adhesion Molecules
0
Nerve Growth Factors
0
Nfasc protein, mouse
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
5709-5723Subventions
Organisme : NINDS NIH HHS
ID : R01 NS043474
Pays : United States
Informations de copyright
Copyright © 2020 the authors.
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