Semin Cell Dev Biol
April 1, 2006;
Apical-basal polarity, Wnt signaling and vertebrate organogenesis.
Wnt proteins elicit several distinct signal transduction cascades and regulate multiple cellular processes that have proven essential for embryonic development in all metazoans investigated. During embryonic development, epithelial cells become polarized along two axes: apical/basal and within the plane of the tissue
. Growing evidence suggests that polarization along each axis is essential for normal embryonic development and that this polarization is regulated in part by the different branches of the Wnt pathway. Here, we review the role of A/B cell
polarity in vertebrate organogenesis with a focus on the involvement of canonical Wnt signaling in this process.
Semin Cell Dev Biol
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Fig. 1. Canonical and PCP/CE Wnt signaling. (A) In canonical signaling, binding
of a Wnt ligand to its receptors results in the repression of the -catenin
destruction complex (GSK-3b, Axin, APC and B-TrCP) which allows -catenin
to accumulate and enter the nucleus where, together with the Lef/Tcfs, it drives
expression of target genes including Wrch-1, Fn and Tiam-1. The canonical and
non-canonical pathways diverge after Dsh with the PCP/CE branch signaling
through Rho, Cdc42 and JNK. (B–D) Genes involved in apical/basal organization
interact with the canonical pathway at several points. Lkb-1 represses
GSK-3b in the absence of Par1 (B), while Par1A activate Dsh in the absence
of Lkb-1 (C). When both Lkb-1 and Par1 are active in the same cell, they are
shuttled away from the Wnt pathway (D). See text for details.
Fig. 2. Molecular control of epithelial organization. (A) Epithelial cells are
divided into three domains: apical, lateral and basal. The junctional complexes
separate the apical from the lateral domains. (B) Several protein complexes interact
to organize the epithelial cell including the apical crumbs complex (purple),
the junctional Par complex (red) and the basolateral scribble complex (yellow).
See text for details.
Fig. 3. The role of aPKC in organogenesis. has and nok mutants lack polarity and are defective in lateral plate mesoderm migration. (A and B) 30 hpf wild type
embryo has correctly polarized LPM with asymmetric migration. (C and D) 30 hpf has and nok mutants show loss of epithelial polarity and defective migration.
(E) Schematic of (A) showing correctly polarized LPM and asymmetric migration. (F) has and nok mutant have identical morphogenetic phenotypes. Used with