Building a tube from solid tissue involves making space between adjacent cells to form a lumen. The two groups recorded similar results about the process, but they started with different goals. Medioni et al. wanted to determine the changes in cell shape and polarity, whereas Santiago-Martínez et al. wanted to know how cells modify their stickiness so they can separate.
Both teams took a close look at the embryonic Drosophila heart, which forms when two rows of cardioblasts converge and flex to produce a hollow cylinder. Medioni et al. performed live imaging with confocal microscopy to follow this cellular choreography, and Santiago-Martínez et al. captured three stages of the process with EM. The groups observed the same changes. Cardioblasts in opposite rows first attach at the top. They then bow outward into a sickle shape and connect at the bottom, leaving a doughnut hole in the middle. The two studies also reached similar conclusions about a pathway that involves the extracellular matrix protein Slit and its receptor, Robo. In effect, the pathway creates a non-stick surface on the lumen side of heart cells.
Santiago-Martínez et al. think that the Slit/Robo pathway works by exiling the protein E-cadherin, which hooks neighboring cells together, from the cells' future lumen surface. Medioni et al. found that cardioblasts with mutant Slit remain round and display an expanded cell-to-cell adhesion domain that holds the lumen closed.