Bursicon functions within the Drosophila CNS to modulate wing expansion behavior, hormone secretion, and cell death.
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.
Peabody
Nathan C
NC
Laboratory of Molecular Biology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, USA.
Diao
Fengqiu
F
Luan
Haojiang
H
Wang
Howard
H
Dewey
Elizabeth M
EM
Honegger
Hans-Willi
HW
White
Benjamin H
BH
D000818:Animals; D030801:Animals, Genetically Modified; D019521:Body Patterning / Q000235:genetics / Q000502:physiology; D016827:CD8 Antigens / Q000378:metabolism; D002116:Calcitonin / Q000378:metabolism; D016923:Cell Death / Q000235:genetics / Q000502:physiology; D002490:Central Nervous System / Q000254:growth & development / Q000378:metabolism*; D004330:Drosophila; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism; D017952:Ganglia, Invertebrate / Q000254:growth & development / Q000378:metabolism; D005786:Gene Expression Regulation / Q000235:genetics; D049452:Green Fluorescent Proteins / Q000235:genetics; D020287:In Situ Nick-End Labeling / Q000379:methods; D007301:Insect Hormones / Q000235:genetics / Q000378:metabolism*; D007447:Invertebrate Hormones / Q000235:genetics / Q000502:physiology*; D007814:Larva; D008675:Metamorphosis, Biological / Q000235:genetics / Q000502:physiology*; D009434:Neural Pathways / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D010446:Peptide Fragments / Q000378:metabolism; D014921:Wings, Animal / Q000502:physiology*
D016827:CD8 Antigens; D029721:Drosophila Proteins; D007301:Insect Hormones; D007447:Invertebrate Hormones; D010446:Peptide Fragments; C485184:enhanced green fluorescent protein; D049452:Green Fluorescent Proteins; C037553:katacalcin; D002116:Calcitonin; C002295:bursicon