Our lab investigates how tissues sense and respond to necrotic injury, a form of unregulated cell death common in disease and trauma. Using the genetically tractable Drosophila wing imaginal disc, we developed models to compare regeneration following necrosis and apoptosis. We discovered that necrotic tissue not only triggers wound-edge signaling but also induces widespread, JNK-independent caspase activity far from the injury—a phenomenon we termed Necrosis-induced Caspase Positive (NiCP) cells. NiCP is essential for regeneration, indicating that signals released from necrotic cells can coordinate repair across large tissue areas.

Our ongoing work reveals that necrotic signaling is spatially and genetically regulated. Necrosis primarily stimulates NiCP in regeneration-competent regions, governed by local WNT and JAK/STAT activity, and results in unique downstream caspase signaling distinct from classical apoptotic programs. These studies show that necrotic cells generate potent, long-range cues that reprogram surviving tissue to promote repair, providing new insight into how destructive injury can paradoxically activate regenerative responses.