| Abstract |
Mechanical forces play critical roles in tissue morphogenesis and homeostasis, yet how tissue mechanics are translated into epithelial cell delamination remains poorly understood. Here, we use the Drosophila pupal wing as an in vivo model to examine how release of tissue tension influences cell death and delamination. Surgical severing of the wing hinge or loss of dumpy (dpy) function alters the force distribution, promotes cell crowding, and thereby significantly increases epithelial cell delamination compared to wild-type controls. An RNAi analysis targeting mechanosensitive components identified Vinculin, an adherens junction-associated force adaptor, as a key suppressor of mechanically induced cell delamination. Both tissue tension release and Vinculin depletion reduced junctional Vinculin levels and elevated Notch transcriptional activity, while canonical Notch transcriptional activation remained undetectable within delaminating cells. In contrast, knockdown of the Notch ligand Delta suppressed cell death and delamination. These findings indicate that release of tissue tension causes changes in forces acting on cells and cell crowding, thereby altering Vinculin-dependent regulation of Delta-Notch signaling and promoting cell delamination through a non-canonical Notch pathway.Key words: cell delamination, mechanotransduction, Delta-Notch pathways.
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