摘要：SummaryThorax fusion occurs in the midline of theDrosophilapupal notum and involves epithelial cell delamination requiring apoptotic signaling. By genetic screening, we found that NADPH oxidases (Nox and Duox) associated with superoxide anion (O˙-2) are responsible for caspase-3 activation and delamination. We observed that Nox is upregulated in cells that undergo delamination and that delamination depends on caspase activation. However, the cell morphology and the almost complete lack of propidium iodide incorporation suggested little membrane disruption and signified apoptotic modulation. These results demonstrate that most delaminating cells undergo caspase activation, but this activation is not sufficient for apoptosis. We showed that the expression ofCatalase, encoding an H2O2scavenger in the cytosol, increases delamination and induces apoptotic nuclear fragmentation in caspase-3-activated cells. These findings suggest that the roles of O˙-2and intracellular H2O2for delamination differs before and after caspase-3 activation, which involves live cell delamination.Graphical AbstractDisplay OmittedHighlights•NADPH oxidases are responsible for cell delamination inDrosophilapupal notum•Nox is upregulated in delaminating cells prior to caspase-3 activation•Nox promotes caspase-3 activation and cell delamination•H2O2suppresses apoptotic nuclear fragmentation during delaminationDevelopmental Genetics; Molecular Genetics
