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Published August 2012 | public
Journal Article

Slits Affect the Timely Migration of Neural Crest Cells Via Robo Receptor

Abstract

Background: Neural crest cells emerge by delamination from the dorsal neural tube and give rise to various components of the peripheral nervous system in vertebrate embryos. These cells change from non-motile into highly motile cells migrating to distant areas before further differentiation. Mechanisms controlling delamination and subsequent migration of neural crest cells are not fully understood. Slit2, a chemorepellant for axonal guidance that repels and stimulates motility of trunk neural crest cells away from the gut has recently been suggested to be a tumor suppressor molecule. The goal of this study was to further investigate the role of Slit2 in trunk neural crest cell migration by constitutive expression in neural crest cells. Results: We found that Slit gain-of-function significantly impaired neural crest cell migration while Slit loss-of-function favored migration. In addition, we observed that the distribution of key cytoskeletal markers was disrupted in both gain and loss of function instances. Conclusions: These findings suggest that Slit molecules might be involved in the processes that allow neural crest cells to begin migrating and transitioning to a mesenchymal type.

Additional Information

© 2012 Wiley Periodicals, Inc. Issue published online: 17 July 2012; Article first published online: 23 JUN 2012; Accepted manuscript online: 11 June 2012 10:51AM EST; Manuscript Accepted: 1 June 2012. We thank Cale Scholl, Kristen Kozak, Shar Alamdari, and Chris Walheim for technical assistance; Ed Laufer for Slits and Robo probes; and Jane Wu for pCS2 plasmids and cell lines. Vivian Lee provided invaluable comments and material during all phases of the work and Betsy Komives, Sonja McKeown, Vincent Lui, and Ui-Soon Khoo critically reviewed the manuscript. This work was supported by an NIH/NINDS AREA grant 1R15-NS060099-01 to M.E.d. B. and NIH SCORE 1SC2GM086312 to M.P.S.

Additional details

Created:
August 22, 2023
Modified:
October 18, 2023