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.
- Developmental Biology 325(2): 363-373 (Journal)
- Registered Authors
- Chandrasekhar, Anand, Halloran, Mary, Maves, Lisa, Sittaramane, Vinoth, Wolman, Marc
- Hindbrain, Motor neuron, Branchiomotor, Neuronal migration, Time-lapse imaging, Cell adhesion molecule, Tag1, Van gogh-like, Laminin, Genetic interaction
- MeSH Terms
- Cell Adhesion
- Cell Adhesion Molecules, Neuronal/physiology*
- Cell Movement
- Contactin 2
- Membrane Proteins/physiology*
- Motor Neurons/physiology*
- Signal Transduction
- Zebrafish Proteins/physiology*
- 19013446 Full text @ Dev. Biol.
Sittaramane, V., Sawant, A., Wolman, M.A., Maves, L., Halloran, M.C., and Chandrasekhar, A. (2009) The cell adhesion molecule Tag1, transmembrane protein Stbm/Vangl2, and Lamininalpha1 exhibit genetic interactions during migration of facial branchiomotor neurons in zebrafish. Developmental Biology. 325(2):363-373.
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.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes