In Drosophila, the larval epithelia require the steroid hormone ecdysone (Ec) secreted from the prothoracic gland for growth; however, upon tissue injury, there is a drop in circulating Ec to redirect developmental pathways towards regenerative growth. It remains unclear how Ec-dependent regeneration can occur despite a low level of Ec in the injured developing larvae. Here, Douglas Terry, Colby Schweibenz and Kenneth Moberg examine the dynamics of Ec during regeneration in wounded Drosophila wing imaginal discs. First, looking at the reporter activity of the Ec receptor (EcR) after genetically-induced injury, the authors find that EcR is active in the surviving cells around the injured site, whereas EcR activity drops in uninjured regions. Then, the authors knock down phantom, disembodied and shade, which are ‘Halloween genes’ that encode enzymes involved in Ec synthesis. They observe that, in the wounded site, EcR expression is reduced when the Halloween genes are knocked down, and the regeneration of injured wing discs is impaired. Finally, they find that the expression of pro-regenerative genes, upd3 and Ets21C, is dependent on local Ec production at the wound. Overall, the findings suggest that injury induces local Ec synthesis at the wounded site to delay development and promote tissue repair in Drosophila.
