ZFIN ID: ZDB-PUB-081121-15
The cell adhesion molecule Tag1, transmembrane protein Stbm/Vangl2, and Lamininalpha1 exhibit genetic interactions during migration of facial branchiomotor neurons in zebrafish
Sittaramane, V., Sawant, A., Wolman, M.A., Maves, L., Halloran, M.C., and Chandrasekhar, A.
Date: 2009
Source: Developmental Biology   325(2): 363-373 (Journal)
Registered Authors: Chandrasekhar, Anand, Halloran, Mary, Maves, Lisa, Sittaramane, Vinoth, Wolman, Marc
Keywords: Hindbrain, Motor neuron, Branchiomotor, Neuronal migration, Time-lapse imaging, Cell adhesion molecule, Tag1, Van gogh-like, Laminin, Genetic interaction
MeSH Terms:
  • Animals
  • Cell Adhesion
  • Cell Adhesion Molecules, Neuronal/physiology*
  • Cell Movement
  • Contactin 2
  • Laminin/physiology*
  • Membrane Proteins/physiology*
  • Motor Neurons/physiology*
  • Rhombencephalon/embryology*
  • Rhombencephalon/physiology
  • Signal Transduction
  • Zebrafish/embryology*
  • Zebrafish/physiology
  • Zebrafish Proteins/physiology*
PubMed: 19013446 Full text @ Dev. Biol.
Interactions between a neuron and its environment play a major role in neuronal migration. We show here that the cell adhesion molecule Transient Axonal Glycoprotein (Tag1) is necessary for the migration of the facial branchiomotor neurons (FBMNs) in the zebrafish hindbrain. In tag1 morphant embryos, FBMN migration is specifically blocked, with no effect on organization or patterning of other hindbrain neurons. Furthermore, using suboptimal morpholino doses and genetic mutants, we found that tag1, lamininalpha1 (lama1) and stbm, which encodes a transmembrane protein Vangl2, exhibit pairwise genetic interactions for FBMN migration. Using time-lapse analyses, we found that FBMNs are affected similarly in all three single morphant embryos, with an inability to extend protrusions in a specific direction, and resulting in the failure of caudal migration. These data suggest that tag1, lama1 and vangl2 participate in a common mechanism that integrates signaling between the FBMN and its environment to regulate migration.