The mechanisms that control shape and rigidity of early embryos are not well understood, and yet are required for all embryonic processes to take place. In the Xenopus blastula, the cortical actin network in each blastomere is required for the maintenance of overall embryonic shape and rigidity. However, the mechanism whereby each cell assembles the appropriate pattern and number of actin filament bundles is not known. The existence of a similar network in each blastomere suggests two possibilities: cell-autonomous inheritance of instructions from the egg; or mutual intercellular signaling mediated by cell contact or diffusible signals. We show that intercellular signaling is required for the correct pattern of cortical actin assembly in Xenopus embryos, and that lysophosphatidic acid (LPA) and its receptors, corresponding to LPA1 and LPA2 in mammals, are both necessary and sufficient for this function.
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