ZFIN ID: ZDB-PUB-070827-2
A Rap GTPase interactor, RADIL, mediates migration of neural crest precursors
Smolen, G.A., Schott, B.J., Stewart, R.A., Diederichs, S., Muir, B., Provencher, H.L., Look, A.T., Sgroi, D.C., Peterson, R.T., and Haber, D.A.
Date: 2007
Source: Genes & Development   21(17): 2131-2136 (Journal)
Registered Authors: Look, A. Thomas, Peterson, Randall, Stewart, Rodney A.
Keywords: Neural crest, migration, adhesion, Rap, development, zebrafish
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Carrier Proteins/physiology*
  • Cell Adhesion/genetics*
  • Cell Movement/genetics*
  • Embryo, Nonmammalian
  • Gene Expression Regulation, Developmental
  • Genes, ras
  • Genes, vpr*
  • Morphogenesis/genetics*
  • Neural Crest/embryology*
  • Zebrafish Proteins/physiology*
  • rap GTP-Binding Proteins/physiology*
PubMed: 17704304 Full text @ Genes & Dev.
The neural crest (NC) is a highly motile cell population that gives rise to multiple tissue lineages during vertebrate embryogenesis. Here, we identify a novel effector of the small GTPase Rap, called RADIL (RA [Ras association] and DIL domains), and show that it is required for cell adhesion and migration. Knockdown of radil in the zebrafish model results in multiple defects in NC-derived lineages such as cartilage, pigment cells, and enteric neurons. We specifically show that these defects are primarily due to the diminished migratory capacity of NC cells. The identification of RADIL as a regulator of NC migration defines a role for the Rap pathway in this process.