Fig. 7.

Model of damage-based tissue communication. Schematic representation of the tissue communication network that is activated following disruptions to muscle homeostasis. Muscle health depends on muscle integrity and the strong attachment of muscle (red) to tendon (green, asterisk) via ECM interactions. Muscle hypercontraction (Damage 1) and weakened MASs that progress to detachment (Damage 2) generate stress responses that activate local and systemic immune responses. Muscle damage prompts a series of cellular immune responses including hemocyte recruitment and melanization. Locally, JAK-STAT signaling is activated in muscle tissue through the binding of Upd ligands to the Domeless (Dome) receptor to induce expression of immune-responsive genes. Toll signaling is activated in conjunction with the JAK-STAT pathway in a reciprocal network. Upon Toll signal transduction, Dl moves into the nuclei of fat body cells to activate Toll-responsive genes such as the AMP, drosomycin. Other forms of cellular stress in muscle tissue or possibly in coordinating tissues such as epithelium (Damage 3) may coincide with destabilization of muscle attachment and contribute to further loss of muscle maintenance.