Fig. 5. Ca²⁺ wave model. A hypothetical model incorporates monocilia, gap junctional communication and polycystin-2 in the vicinity of the node. By analogy with Ca²⁺ waves in certain epithelial and endothelial cells, bending of monocilia on ventral node cells (shown for chick) are proposed to trigger a Ca²⁺ influx, perhaps through polycystin-2 (1), resulting in induction of a second messenger, such as Ins(1,4,5)P₃, (2) that passes through gap junctions to propagate an intercellular Ca²⁺ wave (3) to adjacent cells. The model does not predict whether the Ca²⁺ wave is propagated leftwards, rightwards or both. Directional propagation would provide the simplest link to downstream gene expression and could be achieved in response to signals within the node, for instance if the monocilia sensed the leftward fluid flow [as proposed for the mouse (Tabin and Vogan, 2003)], or by the asymmetric localization of proteins, such as connexins, that are required to receive or propagate the Ca²⁺ signal (see text).