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Published online before print August 17, 2007, 10.1101/gad.1561507
GENES & DEVELOPMENT 21:2131-2136, 2007
©2007 by Cold Spring Harbor Laboratory Press; ISSN 0890-9369/ $5.00
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RESEARCH COMMUNICATIONS

A Rap GTPase interactor, RADIL, mediates migration of neural crest precursors

Gromoslaw A. Smolen1, Benjamin J. Schott1, Rodney A. Stewart2, Sven Diederichs1, Beth Muir3, Heather L. Provencher3, A. Thomas Look2, Dennis C. Sgroi3, Randall T. Peterson4, and Daniel A. Haber1,5

1 Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, Massachusetts 02129, USA; 2 Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA; 3 Department of Pathology, Massachusetts General Hospital, Molecular Pathology Research Unit, Harvard Medical School, Charlestown, Massachusetts 02129, USA; 4 Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA

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.

[Keywords: Neural crest; migration; adhesion; Rap; development; zebrafish]

Received April 12, 2007; revised version accepted July 13, 2007.

6 Corresponding author.

E-MAIL haber{at}helix.mgh.harvard.edu; FAX (617) 724-6919.

Supplemental material is available at http://www.genesdev.org.

Article published online ahead of print. Article and publication date are online at http://www.genesdev.org/cgi/doi/10.1101/gad.1561507


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