During early Xenopus development, embryonic cells assemble a cortical actin network that maintains an embryo's overall shape and rigidity. But how does each cell assemble an appropriately patterned and dense network?Lloyd et al. now report on p. 805 that lysophosphatidic acid (LPA) – a bioactive lipid that influences actin networks and cellular morphology – plays an important role in this process. Their findings show that if the LPA1 and LPA2receptors are overexpressed in the whole frog embryo (LPA2 is newly identified here), denser actin networks develop. Conversely, depleting LPA receptor levels in early embryos reduces network density. When LPA is added to dissociated embryonic cells, or when they are allowed to reaggregate, a denser, more normal actin network replaces the coarser network seen. The authors conclude that intercellular signalling between cells is required to maintain a normally patterned and dense actin network to support the developing embryo, and that this signalling requires LPA.