Fig. 6.

Hypothetical model for the evolution of self-sacrificing gall repair in N. monzeni. (A) Molecular and cellular mechanisms underlying the body fluid clotting for self-sacrificing gall repair by soldier nymphs of N. monzeni. PO, tyrosine, and triglycerides are stored in LGCs, whereas RCP and tyrosine are accumulated in body fluid. The soldier’s body fluid excretion results in immediate formation of a lipidic soft clot and activation of the PO-mediated melanin synthesis cascade. Activated PO converts tyrosine into reactive quinones, which cross-link RCP and other proteins to physically stabilize and harden the clot. (B) General molecular and cellular mechanisms of body fluid clotting and wound sealing in insects, in which PO activation, body fluid clotting, and hemocyte aggregation play pivotal roles. (C) Hypothetical evolutionary scenario for gall-repairing soldier nymphs of N. monzeni, in which preexisting clotting mechanisms are extremely exaggerated—PO drastically up-regulated, tyrosine overproduced, and specialized LGCs proliferated—to cause massive clotting outside the insect body. (D) Self-sacrificing gall repair by soldier nymphs of N. monzeni, in which body fluid clotting mechanisms at the individual level are coopted for social defense at the colony level.