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The Journal of Neuroscience, December 31, 2008, 28(53):14379-14391; doi:10.1523/JNEUROSCI.2842-08.2008

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Cellular/Molecular
Bursicon Functions within the Drosophila CNS to Modulate Wing Expansion Behavior, Hormone Secretion, and Cell Death

Nathan C. Peabody,^1 * Fengqiu Diao,^1 * Haojiang Luan,¹ Howard Wang,¹ Elizabeth M. Dewey,² Hans-Willi Honegger,² and Benjamin H. White¹

¹Laboratory of Molecular Biology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, and ²Department of Biological Sciences, Vanderbilt University, Nashville, Tennessee 37325

Correspondence should be addressed to Benjamin H. White, National Institute of Mental Health, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892. Email: benjaminwhite{at}mail.nih.gov

Hormones are often responsible for synchronizing somatic physiological changes with changes in behavior. Ecdysis (i.e., the shedding of the exoskeleton) in insects has served as a useful model for elucidating the molecular and cellular mechanisms of this synchronization, and has provided numerous insights into the hormonal coordination of body and behavior. An example in which the mechanisms have remained enigmatic is the neurohormone bursicon, which, after the final molt, coordinates the plasticization and tanning of the initially folded wings with behaviors that drive wing expansion. The somatic effects of the hormone are governed by bursicon that is released into the blood from neurons in the abdominal ganglion (the B_AG), which die after wing expansion. How bursicon induces the behavioral programs required for wing expansion, however, has remained unknown. Here we show by targeted suppression of excitability that a pair of bursicon-immunoreactive neurons distinct from the B_AG and located within the subesophageal ganglion in Drosophila (the B_SEG) is involved in controlling wing expansion behaviors. Unlike the B_AG, the B_SEG arborize widely in the nervous system, including within the abdominal neuromeres, suggesting that, in addition to governing behavior, they also may modulate the B_AG. Indeed, we show that animals lacking bursicon receptor function have deficits both in the humoral release of bursicon and in posteclosion apoptosis of the B_AG. Our results reveal novel neuromodulatory functions for bursicon and support the hypothesis that the B_SEG are essential for orchestrating both the behavioral and somatic processes underlying wing expansion.

Key words: ecdysis; eclosion; network; circuit; apoptosis; Drosophila

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Received June 20, 2008; revised Nov. 9, 2008; accepted Nov. 12, 2008.

Correspondence should be addressed to Benjamin H. White, National Institute of Mental Health, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892. Email: benjaminwhite{at}mail.nih.gov

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