Mutations in genes encoding ion channels cause severe defects in development across species but the underlying mechanisms, particularly in tissues other than neurons and muscle, have remained unclear. On p. 2771, Emily Anne Bates and colleagues describe a role for Irk2, an inwardly rectifying potassium channel in Drosophila orthologous to Kir2.1 in vertebrates, in regulating the release of the BMP family morphogen Dpp during development of the wing epithelium. Building on their previous finding that a dominant-negative Irk2 reduces Dpp signalling and causes wing defects, they now show that human KIR2.1 can substitute for inhibited Drosophila Irk2, and that Irk2’s role is restricted to the cells that produce, rather than just transduce, the Dpp signal. Surprisingly, inhibiting Irk2 broadens the distribution of Dpp in the wing, but also alters the dynamics of Dpp release from cells, suggesting that Irk2 controls the timing of Dpp secretion. Irk2 inhibition reduces the amplitude of calcium spikes in wing cells, and depolarising the membrane with extracellular potassium leads to an overall increased release of Dpp, implicating Irk2’s regulation of membrane potential in Dpp release. Together, these results suggest that ion channels influence tissue morphogenesis by regulating the release of morphogens from the membrane.
