College of the Atlantic
Wound-induced polyploidization is dependent on Integrin-Hippo signaling
A key step in tissue repair is to replace cells that have been lost or damaged by injury. One strategy occurs when cell numbers are restored through proliferation. Another occurs when cell size is increased through polyploidization. Studies in Drosophila and vertebrate tissues have demonstrated that polyploid cells arise in adult tissues, at least in part, to promote tissue repair and restore tissue mass. However, the signals that cause polyploid cells to form in response to injury remain poorly understood. In the adult Drosophilaepithelium, polyploid cells are generated by both cell fusion and endoreplication resulting in a giant polyploid syncytium that is essential for wound repair. Here, we identify the β1-Integrin, Myospheroid (Mys) as an activator of wound-induced polyploidization. Mys is upregulated 2.5 fold in the wound-induced polyploid cells, and epithelial specific knockdown results in a significant defect in endoreplication. In addition, we found that Mys signals through the Hippo pathway to regulate Yki targets, including myc. In conclusion, we found that integrin-mediated mechanotransduction is critical to initiate polyploid cell growth.