During the cellularisation step of Drosophila morphogenesis, numerous plasma-membrane furrows extend progressively into the syncytial embryo. Ingression is led by the furrow canal, a discrete F-actin- and Myosin-2-rich compartment that forms at the tip of each new furrow. The mechanisms that partition proteins into the furrow-canal compartment have been unclear, although the basal junctions that flank the compartment have been proposed to have a key role. On page 1815, however, Anna Marie Sokac and Eric Wieschaus show that furrow-canal compartmentalisation progresses normally in a Drosophila mutant that is deficient in Armadillo (a basal-junction component). By contrast, embryos treated with the F-actin-destabilising drug cytochalasin-D have defects in furrow-canal formation that echo the phenotype of the well-characterised nulloX cellularisation mutant: Myosin 2 is missing from some furrow canals (which leads to furrow regression) and markers of adjacent regions of the furrow are present in the furrow canal. The authors propose that actin polymerisation, regulated by Nullo, is central to furrow-canal formation and stabilisation, and therefore to cellularisation.