Snail family genes encode DNA binding zinc finger proteins that act as tran
scriptional repressors. Mouse embryos deficient for the Snail (Sna) gene ex
hibit defects in the formation of the mesoderm germ layer. In Sna(-/-) muta
nt embryos, a mesoderm layer forms and mesodermal marker genes are induced
but the mutant mesoderm is morphologically abnormal. Lacunae form within th
e mesoderm layer of the mutant embryos, and cells lining these lacunae reta
in epithelial characteristics. These cells resemble a columnar epithelium a
nd have apical-basal polarity, with microvilli along the apical surface and
intercellular electron-dense adhesive junctions that resemble adherens jun
ctions. E-cadherin expression is retained in the mesoderm of the Sna(-/-) e
mbryos. These defects are strikingly similar to the gastrulation defects ob
served in snail-deficient Drosophila embryos, suggesting that the mechanism
of repression of E-cadherin transcription by Snail family proteins may hav
e been present in the metazoan ancestor of the arthropod and mammalian line
ages.