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First published online June 1, 2005
doi: 10.1242/10.1242/dev.01866
1 Division of Developmental Biology, Cincinnati Children's Research Foundation,
3333 Burnet Avenue, Cincinnati, OH 45229, USA
2 Physician Scientist Training Program, University of Cincinnati College of
Medicine, University of Cincinnati College of Medicine, PO Box 670555,
Cincinnati, OH 45267, USA
Author for correspondence (e-mail:
christopher.wylie{at}cchmc.org)
Accepted 18 April 2005
As the fertilized Xenopus egg undergoes sequential cell divisions to form a blastula, each cell develops a network of cortical actin that provides shape and skeletal support for the whole embryo. Disruption of this network causes loss of shape and rigidity of the embryo, and disrupts gastrulation movements. We previously showed that lysophosphatidic acid (LPA) signaling controls the change in cortical actin density that occurs at different stages of the cell cycle. Here, we use a gain-of-function screen, using an egg cDNA expression library, to identify an orphan G protein-coupled cell-surface receptor (XFlop) that controls the overall amount of cortical F-actin. Overexpression of XFlop increases the amount of cortical actin, as well as embryo rigidity and wound healing, whereas depletion of maternal XFlop mRNA does the reverse. Both overexpression and depletion of XFlop perturb gastrulation movements. Reciprocal rescue experiments, and comparison of the effects of their depletion in early embryos, show that the XLPA and XFlop signaling pathways play independent roles in cortical actin assembly, and thus that multiple signaling pathways control the actin skeleton in the blastula.
Key words: Cortical actin, G protein coupled receptor, Xenopus
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