title: The leucokinin pathway and its neurons regulate meal size in Drosophila.
abstract: BACKGROUND
  Total food intake is a function of meal size and meal frequency, and adjustments to these parameters allow animals to maintain a stable energy balance in changing environmental conditions. The physiological mechanisms that regulate meal size have been studied in blowflies but have not been previously examined in Drosophila.
  
  
  RESULTS
  Here we show that mutations in the leucokinin neuropeptide (leuc) and leucokinin receptor (lkr) genes cause phenotypes in which Drosophila adults have an increase in meal size and a compensatory reduction in meal frequency. Because mutant flies take larger but fewer meals, their caloric intake is the same as that of wild-type flies. The expression patterns of the leuc and lkr genes identify small groups of brain neurons that regulate this behavior. Leuc-containing presynaptic terminals are found close to Lkr neurons in the brain and ventral ganglia, suggesting that they deliver Leuc peptide to these neurons. Lkr neurons innervate the foregut. Flies in which Leuc or Lkr neurons are ablated have defects identical to those of leucokinin pathway mutants.
  
  
  CONCLUSIONS
  Our data suggest that the increase in meal size in leuc and lkr mutants is due to a meal termination defect, perhaps arising from impaired communication of gut distension signals to the brain. Leucokinin and the leucokinin receptor are homologous to vertebrate tachykinin and its receptor, and injection of tachykinins reduces food consumption. Our results suggest that the roles of the tachykinin system in regulating food intake might be evolutionarily conserved between insects and vertebrates.
authors.affiliation: Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA. alanzi@caltech.edu
authors.forename: Bader
authors.initials: B
authors.lastname: Al-Anzi
authors.forename: Elena
authors.initials: E
authors.lastname: Armand
authors.forename: Paul
authors.initials: P
authors.lastname: Nagamei
authors.forename: Margaret
authors.initials: M
authors.lastname: Olszewski
authors.forename: Viveca
authors.initials: V
authors.lastname: Sapin
authors.forename: Christopher
authors.initials: C
authors.lastname: Waters
authors.forename: Kai
authors.initials: K
authors.lastname: Zinn
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Wyman
authors.forename: Seymour
authors.initials: S
authors.lastname: Benzer
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism*; D004331:Drosophila melanogaster / Q000033:anatomy & histology / Q000502:physiology*; D004435:Eating / Q000502:physiology*; D005247:Feeding Behavior / Q000502:physiology*; D015870:Gene Expression; D008297:Male; D009154:Mutation; D009474:Neurons / Q000166:cytology / Q000378:metabolism*; D009479:Neuropeptides / Q000235:genetics / Q000378:metabolism*; D018013:Receptors, Neuropeptide / Q000235:genetics / Q000378:metabolism; D011993:Recombinant Fusion Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: D029721:Drosophila Proteins; C468143:Lk protein, Drosophila; D009479:Neuropeptides; D018013:Receptors, Neuropeptide; D011993:Recombinant Fusion Proteins; C468144:drosokinin receptor