Affiliation:
1. The Jackson Laboratory, Bar Harbor, Maine 04609
Abstract
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.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Cited by
526 articles.
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