Abstract
SignificanceWe explore mechanisms by which stress caused by acute injury affects blood cell development and inflammatory response in Drosophila. Similar to their mammalian myeloid counterparts, these cells are predisposed to sense and react to sterile injury at distant sites. Upon sterile injury, a breach of epidermis sets up a reactive oxygen species-based signal that bypasses the pathogen-sensing apparatus of septic immune challenge, but merges downstream to activate Toll. A number of autonomous and nonautonomous signaling pathways follow in a sequence and are mapped temporally by the appearance of their corresponding molecular phenotypes. A cell-type that fights deposited parasitic wasp eggs appears with sterile injury without the immune challenge, perhaps in anticipation, because in nature injury is usually followed by infection.
