Meeting Abstract
Tissue damage results in developmental delays in many organisms, putatively by delaying key developmental hormones, allowing for tissue repair. This is noted as pubertal delays in humans and metamorphic delays in holometabolous insects like the tobacco hornworm, Manduca sexta and the fruit fly, Drosophila melanogaster. Understanding how these delays arise can provide insight into how conserved the mechanisms of tissue repair are across animals. The aim of this study was to identify a “critical window” where tissue damage no longer caused delays in development in M. sexta. Larvae were irradiated with varying doses of x-rays at the beginning of the 3rd and during their last larval instar (L5), on days 1, 2, 3 or 4 after ecdysis. Timing to wandering behavior, pupation and adult eclosion were monitored. It was hypothesized that irradiation would delay pupal development if presented early in the last larval instar, but not later – after release of developmental hormones – and that larval molts would not be affected given the differences in the roles of developmental hormones at this time. Pupation was delayed after irradiation at the 3rd larval instar or at the beginning of the 5th larval instar within the 1st day after L5 ecdysis. Adult eclosion was significantly delayed irrespective of when the x-rays were administered. Delays in L3 larvae were only noted at higher irradiation levels. These results suggest a delay factor may inhibit key developmental hormones for pupation that are already released in the L5 stage after day 1. These delay factors, even when released at an earlier instar, will delay pupation and adult eclosion, but not larval molts. These data suggest the effects of tissue damage can have profoundly different results depending on the endocrine status of the organism.
