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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Wnt/Frizzled Signaling Controls C. elegans Gastrulation by Activating Actomyosin Contractility.

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.[1]

References

  1. Wnt/Frizzled Signaling Controls C. elegans Gastrulation by Activating Actomyosin Contractility. Lee, J.Y., Marston, D.J., Walston, T., Hardin, J., Halberstadt, A., Goldstein, B. Curr. Biol. (2006) [Pubmed]
 
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