PUBLICATION

Dock1 functions in Schwann cells to regulate development, maintenance, and repair

Authors
Doan, R.A., Monk, K.R.
ID
ZDB-PUB-250320-1
Date
2025
Source
The Journal of cell biology   224: (Journal)
Registered Authors
Monk, Kelly
Keywords
none
MeSH Terms
  • rac1 GTP-Binding Protein*/genetics
  • rac1 GTP-Binding Protein*/metabolism
  • Neuropeptides
  • Guanine Nucleotide Exchange Factors/genetics
  • Guanine Nucleotide Exchange Factors/metabolism
  • rac GTP-Binding Proteins/genetics
  • rac GTP-Binding Proteins/metabolism
  • Animals
  • Zebrafish Proteins*/genetics
  • Zebrafish Proteins*/metabolism
  • Myelin Sheath*/metabolism
  • Signal Transduction
  • Zebrafish*/genetics
  • Zebrafish*/metabolism
  • Nerve Regeneration/genetics
  • Schwann Cells*/metabolism
  • Mice
PubMed
40105697 Full text @ J. Cell Biol.
Abstract
Schwann cells, the myelinating glia of the peripheral nervous system (PNS), are critical for myelin development, maintenance, and repair. Rac1 is a known regulator of radial sorting, a key step in developmental myelination. Previously, in zebrafish, we showed that the loss of Dock1, a Rac1-specific guanine nucleotide exchange factor, resulted in delayed peripheral myelination during development. Here, we demonstrate that Dock1 is necessary for myelin maintenance and remyelination after injury in adult zebrafish. Furthermore, Dock1 performs an evolutionarily conserved role in mice, functioning cell autonomously in Schwann cells to regulate the development, maintenance, and repair of peripheral myelin. Pharmacological and genetic manipulation of Rac1 in larval zebrafish, along with the analysis of active Rac1 levels in developing Dock1 mutant mouse nerves, revealed an interaction between these two proteins. We propose that the interplay between Dock1 and Rac1 signaling in Schwann cells is required to establish, maintain, and facilitate repair and remyelination within the PNS.
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