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The mouse snail gene encodes a key regulator of the epithelial-mesenchymal transition.

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.

Pubmed ID: 11689706

Authors

  • Carver EA
  • Jiang R
  • Lan Y
  • Oram KF
  • Gridley T

Journal

Molecular and cellular biology

Publication Data

December 5, 2001

Associated Grants

  • Agency: NCI NIH HHS, Id: CA09217
  • Agency: NCI NIH HHS, Id: CA34196
  • Agency: NIDCR NIH HHS, Id: DE13078
  • Agency: NICHD NIH HHS, Id: HD34883

Mesh Terms

  • Abnormalities, Multiple
  • Adherens Junctions
  • Animals
  • Cadherins
  • DNA-Binding Proteins
  • Embryo Loss
  • Embryo, Mammalian
  • Epithelium
  • Gene Targeting
  • Mesoderm
  • Mice
  • Mice, Knockout
  • Mice, Mutant Strains
  • Phenotype
  • RNA, Messenger
  • Transcription Factors
  • Zinc Fingers