First published online April 13, 2007
Development 134, 904e (2007)
© The Company of Biologists Limited
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.
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]
