How a channel springs open

ntercalation—the slotting of cells in between one another—is an established method for converting short and fat into long and slim. This is all very well in slippery, adhesion-sparse mesenchymal tissues. But many such extension events occur in epithelial tissues, where cells are glued together by adhesion complexes. Claire Bertet, Lawrence Sulak, and Thomas Lecuit (IBDM, Marseille, France) now report that epithelial intercalation relies on some strategic tugging by myosin that remodels junctions. The French group expected that extension in fly embryos would involve a few individual motile cells nosing between other stationary cells. Instead they saw “a global and ordered reorganization,” says Lecuit. Borders between cells that lay anterior and posterior to each other contracted to a point. Perpendicular expansion of this point generated a border between dorsal and ventral cells, thus pushing the anterior cell more anterior and the posterior cell more posterior. Extension was therefore achieved by a geometrical shuffling of the original hexagonal arrangement. Myosin II was concentrated near the shrinking (anterior– posterior) membranes and reduced near the expanding (dorsal– ventral) membranes. In embryos with less myosin II, junctions froze and intercalation failed. Myosin need only destabilize adhesion proteins at anterior–posterior membranes, as junction proteins are naturally very dynamic. I