Molecular and Cellular Biology, December 2001, p. 8184-8188, Vol. 21, No. 23
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.23.8184-8188.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


The Jackson Laboratory, Bar Harbor, Maine 04609
Received 2 August 2001/Accepted 28 August 2001
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.
Present address: Center for Oral Biology and Department of Biology,
University of Rochester, Rochester, NY 14642.
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