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J. Cell Biol.,
Volume 141, Number 1, April 6, 1998 297-308


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* Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109; During morphogenesis of the Caenorhabditis
elegans embryo, hypodermal (or epidermal) cells migrate to enclose the embryo in an epithelium and, subsequently, change shape coordinately to elongate the body
(Priess, J.R., and D.I. Hirsh. 1986. Dev. Biol. 117:156-
173; Williams-Masson, E.M., A.N. Malik, and J. Hardin. 1997. Development [Camb.]. 124:2889-2901). We have
isolated mutants defective in morphogenesis that identify three genes required for both cell migration during
body enclosure and cell shape change during body elongation. Analyses of hmp-1, hmp-2, and hmr-1 mutants suggest that products of these genes anchor contractile
actin filament bundles at the adherens junctions between
hypodermal cells and, thereby, transmit the force of bundle contraction into cell shape change. The protein products of all three genes localize to hypodermal adherens
junctions in embryos. The sequences of the predicted
HMP-1, HMP-2, and HMR-1 proteins are related to the
cell adhesion proteins
Program in Cellular and
Molecular Biology, § Department of Zoology, University of Wisconsin, Madison, Wisconsin 53706;
Howard Hughes Medical
Institute; and ¶ Molecular and Cellular Biology Program, ** Department of Zoology, University of Washington, Seattle,
Washington 98195
-catenin,
-catenin/Armadillo,
and classical cadherin, respectively. This putative catenin-cadherin system is not essential for general cell adhesion in the C. elegans embryo, but rather mediates specific aspects of morphogenetic cell shape change and
cytoskeletal organization.
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