ZFIN ID: ZDB-PUB-111027-22
Netrin Signaling Breaks the Equivalence between Two Identified Zebrafish Motoneurons Revealing a New Role of Intermediate Targets
Hale, L.A., Fowler, D.K., and Eisen, J.S.
Date: 2011
Source: PLoS One 6(10): e25841 (Journal)
Registered Authors: Eisen, Judith S., Hale, Laura
Keywords: Pioneer axons, Embryos, Axons, Neurons, Zebrafish, Axon guidance, Spinal cord, Muscle biochemistry
MeSH Terms:
  • Animals
  • Axons/metabolism
  • Base Sequence
  • Cell Differentiation
  • Cell Movement
  • Cell Survival
  • Gene Expression Regulation
  • Gene Knockdown Techniques
  • Motor Neurons/cytology*
  • Motor Neurons/metabolism*
  • Motor Neurons/physiology
  • Muscles/metabolism
  • Nerve Growth Factors/deficiency
  • Nerve Growth Factors/genetics
  • Nerve Growth Factors/metabolism*
  • Receptors, Cell Surface/metabolism
  • Synapses/metabolism
  • Synapses/physiology
  • Tumor Suppressor Proteins/deficiency
  • Tumor Suppressor Proteins/genetics
  • Tumor Suppressor Proteins/metabolism*
  • Zebrafish/metabolism*
  • Zebrafish/physiology
  • Zebrafish Proteins/deficiency
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 22003409 Full text @ PLoS One


We previously showed that equivalence between two identified zebrafish motoneurons is broken by interactions with identified muscle fibers that act as an intermediate target for the axons of these motoneurons. Here we investigate the molecular basis of the signaling interaction between the intermediate target and the motoneurons.

Principal Findings

We provide evidence that Netrin 1a is an intermediate target-derived signal that causes two equivalent motoneurons to adopt distinct fates. We show that although these two motoneurons express the same Netrin receptors, their axons respond differently to Netrin 1a encountered at the intermediate target. Furthermore, we demonstrate that when Netrin 1a is knocked down, more distal intermediate targets that express other Netrins can also function to break equivalence between these motoneurons.


Our results suggest a new role for intermediate targets in breaking neuronal equivalence. The data we present reveal that signals encountered during axon pathfinding can cause equivalent neurons to adopt distinct fates. Such signals may be key in diversifying a neuronal population and leading to correct circuit formation.