A Rap GTPase interactor, RADIL, mediates migration of neural crest precursors.
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, 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.
Smolen
Gromoslaw A
GA
Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Schott
Benjamin J
BJ
Stewart
Rodney A
RA
Diederichs
Sven
S
Muir
Beth
B
Provencher
Heather L
HL
Look
A Thomas
AT
Sgroi
Dennis C
DC
Peterson
Randall T
RT
Haber
Daniel A
DA
D000818:Animals; D030801:Animals, Genetically Modified; D002352:Carrier Proteins / Q000502:physiology*; D002448:Cell Adhesion / Q000235:genetics*; D002465:Cell Movement / Q000235:genetics*; D004625:Embryo, Nonmammalian; D018507:Gene Expression Regulation, Developmental; D011905:Genes, ras; D016334:Genes, vpr; D009024:Morphogenesis / Q000235:genetics*; D009432:Neural Crest / Q000196:embryology*; D029961:Zebrafish Proteins / Q000502:physiology*; D020668:rap GTP-Binding Proteins / Q000502:physiology*
D002352:Carrier Proteins; C523884:RADIL protein, zebrafish; D029961:Zebrafish Proteins; D020668:rap GTP-Binding Proteins
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