Abstract

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

Keywords

MesodermBiologyCell biologyGastrulationGerm layerSnailAdherens junctionEpiblastEctodermIngressionEndodermGeneticsCadherinMolecular biologyEmbryoGeneEmbryogenesisCellular differentiationEmbryonic stem cell

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Year
2001
Type
article
Volume
21
Issue
23
Pages
8184-8188
Citations
615
Access
Closed

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Ethan A. Carver, Rulang Jiang, Yu Lan et al. (2001). The Mouse Snail Gene Encodes a Key Regulator of the Epithelial-Mesenchymal Transition. Molecular and Cellular Biology , 21 (23) , 8184-8188. https://doi.org/10.1128/mcb.21.23.8184-8188.2001

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DOI
10.1128/mcb.21.23.8184-8188.2001