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J. Cell Biol.,
Volume 139, Number 4, November 17, 1997 1033-1046
-Catenin Mutant, and of the
Wnt-signaling Pathway by -Catenin in Xenopus Embryos
* Cell Biology Program, Department of Biochemistry and Biophysics, and Howard Hughes Medical Institute, University
of California, San Francisco, California 94143-0724; and In Xenopus laevis development, We next show that coexpression of Cellular Biochemistry and Biophysics Program, Memorial
Sloan-Kettering Cancer Center, New York 10021
-catenin
plays an important role in the Wnt-signaling pathway
by establishing the Nieuwkoop center, which in turn
leads to specification of the dorsoventral axis. Cadherins are essential for embryonic morphogenesis since they mediate calcium-dependent cell-cell adhesion and
can modulate -catenin signaling. 
-catenin links
-catenin to the actin-based cytoskeleton. To study the
role of endogenous -catenin in early development, we
have made deletion mutants of N-catenin. The binding domain of -catenin has been mapped to the NH2-terminal 210 amino acids of N-catenin. Overexpression of mutants lacking the COOH-terminal 230 amino
acids causes severe developmental defects that reflect
impaired calcium-dependent blastomere adhesion. Lack of normal adhesive interactions results in a loss of
the blastocoel in early embryos and ripping of the ectodermal layer during gastrulation. The phenotypes of
the dominant-negative mutants can be rescued by coexpressing full-length N-catenin or a mutant of -catenin that lacks the internal armadillo repeats.
N-catenin antagonizes the dorsalizing effects of -catenin and Xwnt-8.
This can be seen phenotypically, or by studying the effects of expression on the downstream homeobox gene
Siamois. Thus, -catenin is essential for proper morphogenesis of the embryo and may act as a regulator of
the intracellular -catenin signaling pathway in vivo.
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