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First published online October 26, 2007
doi: 10.1242/10.1242/dev.006858



1 Instituto Cajal, CSIC, Doctor Arce 37, 28002 Madrid, Spain.
2 Instituto de Neurociencias de Alicante, CSIC-UMH, Apartado 18, Sant Joan
d'Alacant, 03550 Spain.
3 Millennium Nucleus in Developmental Biology, Facultad de Ciencias, Universidad
de Chile, Santiago, Chile.
4 Department of Anatomy and Developmental Biology, University College London,
London, UK.
Author for correspondence (e-mail:
anieto{at}umh.es)
Accepted 29 August 2007
The Snail genes are implicated in processes that involve cell movement, both during embryonic development and tumour progression. In teleosts, the vertebrate Snail1 gene is represented by two distinct genes, snail1a and snail1b (previously snail1 and snail2). These genes are expressed in complementary mesodermal domains and their combined expression matches that of their mammalian counterpart. By analysing their loss and gain of function, we found that the most-anterior axial mesendodermal cells, the precursors of the polster, move in a cohesive manner directed by the activity of snail1a- and snail1b-expressing cells surrounding these precursors. The cell-autonomous function of Snail1 proteins regulates cell motility and influences the behaviour of Snail-negative neighbouring cells. Snail1a is required by the prechordal plate for it to reach its normal position, whereas Snail1b controls the acquisition of its normal shape. These non-redundant functions of Snail1a and Snail1b in controlling axial mesendoderm migration comply with the duplication-degeneration-complementation model, and indicate that Snail genes not only act as inducers of epithelial-to-mesenchymal transition, but also as more general regulators of cell adhesion and movement.
Key words: Extension, Prechordal plate, Axial mesendoderm, E-Cadherin, Epithelial-mesenchymal transition, Cell adhesion, Cell migration, DDC model
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