Epithelial cell delamination – the process by which individual epithelial cells detach from an epithelial layer – is a common phenomenon throughout development and can be observed across a wide range of species. Despite its prevalence, it remains unclear whether the mechanism that drives single-cell delamination varies according to the context and, if so, how. In this issue (p. 2153), Yan Yan and colleagues investigate the mechanism of neuroblast delamination in the Drosophila embryo and find that it differs to that previously reported for epithelial homeostasis. Using an elegant combination of live imaging, genetics, pharmacology and mathematical modelling, the authors describe a new mechanism for cell delamination in which the neuroblasts undergo incremental apical constriction, which coincides with pulses of myosin accumulation at their medial apical cortex. By contrast, the accumulation of junctional myosin only has a weak correlation with apical constriction.
The authors demonstrate that the quantitative difference in the frequency and magnitude of myosin pulses critically determines whether a cell will effectively constrict, and further provide evidence for the possibility that this is regulated by the same signal that defines the neuroblast cell fate, namely, Notch. This study establishes a mechanism for cell delamination that is distinct from the previously reported mechanism, and opens up a new area of research into the possibility of Notch signalling upstream of dynamic cytoskeletal rearrangements.
