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First published online April 13, 2007

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Palatal fusion at a Snail's pace

The role of Snail proteins in patterning vertebrate embryos is varied and widely documented. They regulate epithelial-mesenchymal transitions by downregulating epithelial-specific genes and are involved in other cellular processes, such as neural crest delamination. Thomas Gridley's group now report that, surprisingly, Snai1 and Snai2, encoding Snail and Slug, respectively, have no apparent role in neural crest generation or delamination in mice, but are crucial for proper craniofacial morphogenesis (p. 1789). They show that the deletion of both copies of Snai1 in embryonic neural crest cells performed on a null Snai2 genetic background results in multiple craniofacial defects, and a cleft palate defect that is very different from that seen in Snai1^+/- Snai2^-/- mouse embryos. This cleft palate defect arises from the failure of Meckel's cartilage to extend the mandible, a condition also seen in humans with Pierre Robin Sequence, in which a smaller mandible prevents the correct positioning of the tongue. As such, these mice provide a useful model in which to study this developmental disorder.

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Related articles in Development:

Multiple functions of Snail family genes during palate development in mice

Stephen A. Murray, Kathleen F. Oram, and Thomas Gridley
Development 2007 134: 1789-1797. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?