Insect growth is punctuated by molts, during which the animal produces a new exoskeleton. The molt culminates with ecdysis, an ordered sequence of behaviors that causes the old cuticle to be shed. This sequence is activated by Ecdysis Triggering Hormone (ETH), which acts on the CNS to activate neurons that produce neuropeptides implicated in ecdysis, including Eclosion hormone (EH), Crustacean Cardioactive Peptide (CCAP), and bursicon. Despite over 40 years of research on ecdysis, our understanding of the precise roles of these neurohormones remains rudimentary. Of particular interest is EH, whose role beyond the well-accepted action of massively upregulating ETH release has remained elusive. We report on the isolation of an eh null mutant in Drosophila, and use it to investigate the role of EH in larval ecdysis. We found that null mutant animals invariably died at around the time of ecdysis, revealing an essential role in its control. Unexpectedly, however, they failed to express the preparatory behavior of pre-ecdysis while directly expressing the motor program of ecdysis. In addition, although ETH release could not be detected in these animals, the lack of pre-ecdysis could not be rescued by injections of ETH, suggesting that EH is required within the CNS for ETH to trigger the normal ecdysial sequence. Using a genetically-encoded calcium probe we show that EH configures the response of the CNS to ETH. These findings show that EH plays an essential role in the Drosophila CNS in the control of ecdysis, in addition to its known role in the periphery of triggering ETH release.
Genetic analysis of Eclosion hormone action during Drosophila larval ecdysis
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Eileen Krüger, Wilson Mena, Eleanor C. Lahr, Erik C. Johnson, John Ewer; Genetic analysis of Eclosion hormone action during Drosophila larval ecdysis. Development 2015; dev.126995. doi: https://doi.org/10.1242/dev.126995
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