Both populations, however, express polycystin-2, a cation channel that acts as a mechanosensor in the kidney, where fluid currents trigger an influx of calcium. When the Yale team looked at calcium signaling in the node, they found that only those cilia to the left of the motile population induce a rise in intracellular calcium. This asymmetric distribution is disrupted in lrd and polycystin-2 mutants, suggesting that nodal flow produced by the central motile cilia induce calcium influx only in cells in the direction of flow.
“The whole nodal flow hypothesis has been somewhat of a difficult sell, because a major developmental process—formation of one of the three primary body axes—is happening in the extraembryonic space,” says Brueckner. “But our model suggests that L–R development is entirely dependent on the physical force created by nodal flow, and its inherent simplicity makes it really satisfying.” The next step is to determine how asymmetrically expressed genes like nodal are regulated by calcium signaling. ▪