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Curr Biol. 2006 Oct 24;16(20):1986-97.

Wnt/Frizzled signaling controls C. elegans gastrulation by activating actomyosin contractility.

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1
Department of Biology, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina 27599-3280, USA.

Abstract

BACKGROUND:

Embryonic patterning mechanisms regulate the cytoskeletal machinery that drives morphogenesis, but there are few cases where links between patterning mechanisms and morphogenesis are well understood. We have used a combination of genetics, in vivo imaging, and cell manipulations to identify such links in C. elegans gastrulation. Gastrulation in C. elegans begins with the internalization of endodermal precursor cells in a process that depends on apical constriction of ingressing cells.

RESULTS:

We show that ingression of the endodermal precursor cells is regulated by pathways, including a Wnt-Frizzled signaling pathway, that specify endodermal cell fate. We find that Wnt signaling has a role in gastrulation in addition to its earlier roles in regulating endodermal cell fate and cell-cycle timing. In the absence of Wnt signaling, endodermal precursor cells polarize and enrich myosin II apically but fail to contract their apical surfaces. We show that a regulatory myosin light chain normally becomes phosphorylated on the apical side of ingressing cells at a conserved site that can lead to myosin-filament formation and contraction of actomyosin networks and that this phosphorylation depends on Wnt signaling.

CONCLUSIONS:

We conclude that Wnt signaling regulates C. elegans gastrulation through regulatory myosin light-chain phosphorylation, which results in the contraction of the apical surface of ingressing cells. These findings forge new links between cell-fate specification and morphogenesis, and they represent a novel mechanism by which Wnt signaling can regulate morphogenesis.

Comment in

PMID:
17055977
PMCID:
PMC2989422
DOI:
10.1016/j.cub.2006.08.090
[Indexed for MEDLINE]
Free PMC Article
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