Our lab explores the molecular logic by which damaged tissues recognize injury and initiate regenerative gene expression programs. Using the genetically tractable Drosophila imaginal disc, we have found that injury-responsive transcription is orchestrated by specialized enhancer elements, known as Damage Responsive Maturity Silenced (DRMS) enhancers that become actived upon tissue damage. These enhancers integrate signals from conserved pathways such as JNK and JAK/STAT to trigger expression of key regenerative genes, including wingless (Drosophila WNT1), Wnt6 and Mmp1. Using precise genetic ablation, we have shown that activation of these enhancers is an early and essential step in rebuilding tissue architecture following injury.

Our findings demonstrate that regenerative activation occurs through modular enhancer organization: one module senses damage and activates transcription through AP-1 binding, while adjacent regions impose context-specific control. By dissecting these enhancer modules, we have defined how local signals re-engage growth and patterning genes only within injured territories. Current work uses the DUAL Control genetic system to ablate tissue and manipulate gene activity within the regenerating blastema, enabling us to test how transcriptional networks collaborate to coordinate wound detection, proliferation, and morphogenesis. Collectively, our research identifies the genetic circuitry that converts damage signals into regenerative gene expression