Figures & data
Figure 1. A Proposed Model for the Injury Response Checkpoint. (A) Synthesis of Ecdysone (E) by the prothoracic cells of the larval Ring Gland is stimulated by PTTH. Citation57–62 PTTH release stimulates production of E which is released into the hemolymph. Citation60 Ecdysone is converted to its active form 20-hydroxyecdysone (20E) by enzymes expressed in target tissues where 20E triggers a series of downstream events leading to developmental progression.87 (B) Tissue damage and regenerating tissues lead to activation of JNK signaling and increased expression of dilp8. Citation22,69 DILP8 disrupts ecdysteroid production by decreasing expression of ecdysteroidogenic enzymes including dib and phm and possibly delaying the PTTH peak. Citation22,69 Tissue damage also influences ptth expression via a retinoid-dependent pathway which is separate from the DILP8 pathway. Citation14,22 Wing imaginal disc damage is associated with decreased expression of the ecdysone receptor and several ecdysone response genes, however it is unclear whether or not this is a direct effect of the injury response signals or a by-product of reduced ecdysteroid production. Citation15 Increased expression of ecdysone oxidase, which encodes an enzyme
