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

  1. Gromoslaw A. Smolen1,
  2. Benjamin J. Schott1,
  3. Rodney A. Stewart2,
  4. Sven Diederichs1,
  5. Beth Muir3,
  6. Heather L. Provencher3,
  7. A. Thomas Look2,
  8. Dennis C. Sgroi3,
  9. Randall T. Peterson4, and
  10. Daniel A. Haber1,5
  1. 1 Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, Massachusetts 02129, USA;
  2. 2 Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA;
  3. 3 Department of Pathology, Massachusetts General Hospital, Molecular Pathology Research Unit, Harvard Medical School, Charlestown, Massachusetts 02129, USA;
  4. 4 Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA

Abstract

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.

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  1. Published in Advance August 17, 2007, doi: 10.1101/gad.1561507 Genes & Dev. 21: 2131-2136 Copyright © 2007, Cold Spring Harbor Laboratory Press

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