Venom-induced alterations in fly lipid metabolism and its impact on larval development of the ectoparasitoid Nasonia vitripennis (Walker) (Hymenoptera: Pteromalidae).
Rivers D.B. | Denlinger D.L.
Parasitism by the ectoparasitoid Nasonia vitripennis suppressed development in three species of carrion-feeding flies (Sarcophaga bullata, Phormia regina, and Sarcodexia sternodontus), but Musca domestica died quickly in response to envenomation, which made this host unsuitable for development of N. vitripennis. More parasitoids were produced on flies showing arrested development than in M. domestica, and species that sustained the longest periods of suppressed development prior to death yielded the highest number of wasp progeny. Lipid levels were altered by envenomation in all fly species, but lipid accumulated in the fat body only in the preferred host, S. bullata. Fat body accumulation occurred concurrently with a decline in the hemolymph lipid titer, suggesting that the utilization/mobilization of fat body lipid was altered. Fat body lipid content could be elevated by parasitism, by envenomation (without egg deposition), or by injection of crude venom, demonstrating that the venom alone was capable of altering fly lipid metabolism. In the presence of feeding parasitoid larvae, the lipid content of S. bullata fat body did not reach the peak titers observed with envenomation alone or by injection of isolated crude venom, thus suggesting that the developing wasp alters the lipid content of the host. This is consistent with the wasp larva's dependence on the timetable of host changes initiated by envenomation. Wasp larvae deposited on the host out of synchrony with the changes that normally follow envenomation were much less successful in developing to adulthood.
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