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THE HORMONAL COORDINATION OF BEHAVIOR AND PHYSIOLOGY AT ADULT ECDYSIS IN DROSOPHILA MELANOGASTER

THE HORMONAL COORDINATION OF BEHAVIOR AND PHYSIOLOGY AT ADULT ECDYSIS IN DROSOPHILA MELANOGASTER,JAMES D. BAKER,SUSAN L. MCNABB,JAMES W. TRUMAN

THE HORMONAL COORDINATION OF BEHAVIOR AND PHYSIOLOGY AT ADULT ECDYSIS IN DROSOPHILA MELANOGASTER   (Citations: 32)
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In insects, ecdysis is thought to be controlled by the interaction between peptide hormones; in particular between ecdysis-triggering hormone (ETH) from the periphery and eclosion hormone (EH) and crustacean cardioactive peptide (CCAP) from the central nervous system. We examined the behavioral and physiological functions of the first two of these peptides in Drosophila melanogaster using wild-type flies and knockout flies that lacked EH neurons. We used ETH from Manduca sexta (MasETH) to induce premature ecdysis and compared the responses of the two types of flies. The final release of EH normally occurs approximately 40 min before ecdysis. It is correlated with cyclic guanosine monophosphate (cGMP) production in selected neurons and tracheae, by an elevation in the heart rate and by the filling of the new tracheae with air. Injection of developing flies with MasETH causes all these events to occur prematurely. In EH cell knockouts, none of these changes occurs in response to MasETH, and these flies show a permanent failure in tracheal filling. This failure can be overcome in the knockouts by injecting them with membrane-permeant analogs of cGMP, the second messenger for EH. The basis for the 40 min delay between EH release and the onset of ecdysis was examined by decapitating flies at various times relative to EH release. In flies that had already released EH, decapitation was always followed within 1 min by the start of ecdysis. Immediate ecdysis was never observed when the EH cell knockout flies were decapitated. We propose that EH activates both ventral central nervous system elements necessary for ecdysis (possibly the CCAP cells) and descending inhibitory neurons from the head. This descending inhibition establishes a delay in the onset of ecdysis that allows the completion of EH-activated physiological processes such as tracheal filling. A waning in the inhibition eventually allows ecdysis to begin 30-40 min later. Summary
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    • ...Flight however is not possible during a critical period immediately after the emergence of a fly from the puparium—a process called eclosion that lasts for only a few seconds (Baker et al. 1999)...

    Sarah Hammondet al. Ontogeny of flight initiation in the fly Drosophila melanogaster : imp...

    • ...Park et al., 2002), rabbit anti-EH (used at 1:150; kindly provided by J. Truman, University of Washington, Seattle, WA), sheep anti-cGMP (used at 1:500) (Baker et al., 1999), and mouse anti-LacZ (used at 1:2000; Promega, Madison, WI)...
    • ...The inability of ETH peptides to consistently cause the premature ecdysis of EH KO animals has been noted previously for adult eclosion (McNabb et al., 1997; Baker et al., 1999) using either Manduca Inka cell extract or MasETH...
    • ...However, EH KO larvae (McNabb et al., 1997; this study) and pharate adults (Baker et al., 1999) also show defects in tracheal air filling...
    • ...Such injections also rescued the defects in respiratory dynamics expressed at adult eclosion by EH KO flies (Baker et al., 1999)...
    • ...Such insensitivity has been noted previously but using Manduca ETH (McNabb et al., 1997; Baker et al., 1999), raising the possibility that it was attributable to differences between the moth and the fly peptides...

    Anthony C. Clarket al. Neuroendocrine Control of Larval Ecdysis Behavior in Drosophila: Compl...

    • ...Studies of eclosion in Drosophila revealed that increases in cGMP were occasionally seen in tracheae that were correlated with the release of EH (Baker et al., 1999)...
    • ...These cGMP increases were absent in animals that lacked the EH containing VM cells suggesting that tracheae are also EH targets (Baker et al., 1999)...

    David B. Mortonet al. Cellular signaling in eclosion hormone action

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