Meeting Abstract
The developmental timing and progression of growth in insects is controlled by neural and endocrine signaling. In particular, the release of 20-hydroxyecdysone (20-HE) from the brain into the hemolymph (blood) stimulates molting at the larval, pupal, and adult stages. It is hypothesized that the release of the endocrine signal that drives development, 20-HE, is inhibited when an insect’s tissue is damaged. Specifically, damage to the imaginal disc tissues of the fruitfly Drosophila melanogaster appears to cause a delay in the release of 20-HE and thus a delay in development. This has not yet been demonstrated in the hornworm Manduca sexta. We hypothesized that injection of a synthetic 20-HE analog (RH 5992) would reduce the developmental delay noted after tissue damage. The hornworm imaginal discs were damaged by exposure to 10 kRads of X-ray irradiation. At a time point when the levels of ecdysteroids were expected to be elevated, hornworms were injected with 2 ul of either 100% ethanol (vehicle) or 0.3mM to 30mM doses of RH 5992 (tebufenozide), a long-acting 20-HE agonist, in control and irradiated larvae. Following treatment, time-lapse photography was used to record timing of pupation. As expected, pupation delays were noted after irradiation in the ethanol-injected irradiated animals. However, irradiated animals that were treated with 0.3 mM – 3mM RH 5992 showed shortened developmental delays, although not to the level of control larvae. Animals that were treated with higher doses of RH 5992 also failed to pupate and eclose correctly. This shows that damage induced development delays can be reduced to some extent by increasing the abundance of ecdysteroids in the hemolymph.
