The rhythm of adult eclosion in Drosophila is one of the most extensively studied rhythms in insects. The final form of the ecdysis rhythm, however, is a product of endogenous time-keeping via the circadian clock and responses to exogenous cues such as the lights-on signal. The latter results in a pronounced skewing of the ecdysis peak just following lights-on. Recent studies in both Drosophila and the moth Manduca have shown that ecdysis is controlled through a complex hormonal cascade that includes the steroid hormone, 20 hydroxyecdysone (20E), and a series of peptide hormones: eclosion hormone (EH), ecdysis-triggering hormone (ETH), and crustacean cardioactive peptide (CCAP). We have been interested in how endogenous and exogenous timing factors impinge on this endocrine control pathway. Through a series of mutations and genetically engineered flies, we have found that endogenous and exogenous factors act through different portions of the control cascade. Removal of the EH neurons renders the ecdysis system incapable of responding to the lights-on signal. Although we originally though that the lights-on signal acted to induce EH release in Drosophila, we now have evidence that this stimulus acts to shorten the delay between EH release and the subsequent release of CCAP. In contrast to the lights-on response, the circadian control of ecdysis in Drosophila does not require the EH neurons. Nor does it apparently require ETH. We think that there is a parallel pathway that can also activate the CCAP neurons -- a prerequisite for ecdysis. This pathway likely involves a circadian control over the timing of the 20E decline at the end of metamorphosis. Evidence for this pathway will be discussed.

Index items: Drosophila melanogaster, circadian rhythms, photoreception