Journal
NATURE NEUROSCIENCE
Volume 17, Issue 12, Pages 1673-1681Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.3858
Keywords
-
Categories
Funding
- US National Institutes of Health [NS069688, NS044916, HL084383, HL083422, HL114383]
- National Multiple Sclerosis Society
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
- Medical Research Council [MR/L011379/1] Funding Source: researchfish
- MRC [MR/L011379/1] Funding Source: UKRI
Ask authors/readers for more resources
Neuron-glia interactions establish functional membrane domains along myelinated axons. These include nodes of Ranvier, paranodal axoglial junctions and juxtaparanodes. Paranodal junctions are the largest vertebrate junctional adhesion complex, and they are essential for rapid saltatory conduction and contribute to assembly and maintenance of nodes. However, the molecular mechanisms underlying paranodal junction assembly are poorly understood. Ankyrins are cytoskeletal scaffolds traditionally associated with Na+ channel clustering in neurons and are important for membrane domain establishment and maintenance in many cell types. Here we show that ankyrin-B, expressed by Schwann cells, and ankyrin-G, expressed by oligodendrocytes, are highly enriched at the glial side of paranodal junctions where they interact with the essential glial junctional component neurofascin 155. Conditional knockout of ankyrins in oligodendrocytes disrupts paranodal junction assembly and delays nerve conduction during early development in mice. Thus, glial ankyrins function as major scaffolds that facilitate early and efficient paranodal junction assembly in the developing CNS.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available