ZFIN ID: ZDB-PUB-161008-2
Cadherin-2 Is Required Cell Autonomously for Collective Migration of Facial Branchiomotor Neurons
Rebman, J.K., Kirchoff, K.E., Walsh, G.S.
Date: 2016
Source: PLoS One   11: e0164433 (Journal)
Registered Authors: Rebman, Jane K., Walsh, Gregory
Keywords: Embryos, Neuron migration, Neurons, Motor neurons, Hindbrain, Axons, Efferent neurons, Zebrafish
MeSH Terms:
  • Adaptor Proteins, Signal Transducing/metabolism
  • Animals
  • Animals, Genetically Modified/metabolism
  • Animals, Genetically Modified/physiology
  • Cadherins/metabolism*
  • Cell Adhesion/physiology
  • Cell Movement/physiology*
  • Cell Polarity/physiology
  • Facial Nerve/physiology*
  • Motor Neurons/metabolism*
  • Motor Neurons/physiology*
  • Promoter Regions, Genetic/physiology
  • Rhombencephalon/embryology
  • Rhombencephalon/metabolism
  • Rhombencephalon/physiology
  • Zebrafish
  • Zebrafish Proteins/metabolism
PubMed: 27716840 Full text @ PLoS One
Collective migration depends on cell-cell interactions between neighbors that contribute to their overall directionality, yet the mechanisms that control the coordinated migration of neurons remains to be elucidated. During hindbrain development, facial branchiomotor neurons (FBMNs) undergo a stereotypic tangential caudal migration from their place of birth in rhombomere (r)4 to their final location in r6/7. FBMNs engage in collective cell migration that depends on neuron-to-neuron interactions to facilitate caudal directionality. Here, we demonstrate that Cadherin-2-mediated neuron-to-neuron adhesion is necessary for directional and collective migration of FBMNs. We generated stable transgenic zebrafish expressing dominant-negative Cadherin-2 (Cdh2ΔEC) driven by the islet1 promoter. Cell-autonomous inactivation of Cadherin-2 function led to non-directional migration of FBMNs and a defect in caudal tangential migration. Additionally, mosaic analysis revealed that Cdh2ΔEC-expressing FBMNs are not influenced to migrate caudally by neighboring wild-type FBMNs due to a defect in collective cell migration. Taken together, our data suggest that Cadherin-2 plays an essential cell-autonomous role in mediating the collective migration of FBMNs.