To cope with inevitable injury, organisms possess efficient wound healing mechanisms to maintain tissue integrity and guard against infection. However, the cellular and molecular details by which wound healing is accomplished remain poorly defined. Drosophila melanogaster serves as a great model organism to study wound healing because of the versatile genetic tools available and the simple anatomy of the epidermal barrier. Upon larval epidermal wounding, epidermal cells around the wound elongate and migrate in the absence of cell division to ultimately close the wound. Using the wound closure assay we established, we found the Hippo downstream transcriptional regulator, Yorkie (Yki) and its TEAD binding partner Scalloped (Sd) to be required for epidermal wound healing. Intriguingly, unlike in other regenerative contexts, Yki does not regulate the balance of mitosis or apoptosis in the healing larval epidermis. Rather, it seems to regulate actin polymerization in the migrating wound-edge epidermal cells. Moreover, with a series of genetic analyses, we found that Yki has a strong genetic interaction with another wound closure signaling, the Jun N-terminal Kinase (JNK) pathway. Our results suggest that there is a positive feedback loop between these two pathways to facilitate proper epidermal wound healing.