title: Manipulation of components that control feeding behavior in Drosophila melanogaster increases sensitivity to amino acid starvation.
abstract: Feeding is a complex behavior that is regulated by several internal mechanisms. Neuropeptides are able to survey quantities of stored energy and inform the organism if nutrient intake is required. In addition to this homeostatic regulation, a post-feeding reward system positively reinforces feeding. Slight adjustments to either system can tilt the balance to affect the energy reserves and survivorship in times of nutrient adversity. Neuropeptide F (NPF), a homolog of the mammalian neuropeptide Y, acts to induce feeding within the homeostatic regulation of this behavior. Drosophila and other insects bear a shorter form of NPF known as short NPF (sNPF) that can influence feeding. A neural hormone regulator, the dopamine transporter (DAT), works to clear dopamine from the synapses. This action may manipulate the post-feeding reward circuit in that lowered dopamine levels depress feeding, and excess dopamine levels encourage feeding. Here, we have overexpressed and impaired the activities of NPF, sNPF, and DAT in Drosophila, and we examined their ability to survive during conditions of amino acid starvation. Too much or too little NPF or sNPF, which are key players in homeostatic feeding regulation, leads to increased sensitivity to amino acid starvation and diminished survivorship when compared to controls. When DAT, a member of the post-feeding reward system, is either overexpressed or reduced via mutation, Drosophila has increased sensitivity to amino acid starvation. Taken together, these results indicate that subtle variation in the expression of key components of these systems impacts survivorship during adverse nutrient conditions.
authors.affiliation: Department of Biology, Elizabeth Avenue, Science Building, Memorial University of Newfoundland, St. John's, Newfoundland and Labrador, Canada.
authors.forename: J D
authors.initials: JD
authors.lastname: Slade
authors.affiliation: Department of Biology, Elizabeth Avenue, Science Building, Memorial University of Newfoundland, St. John's, Newfoundland and Labrador, Canada.
authors.forename: B E
authors.initials: BE
authors.lastname: Staveley
mesh_terms: D000596:Amino Acids / Q000172:deficiency* / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism; D050483:Dopamine Plasma Membrane Transport Proteins / Q000235:genetics* / Q000378:metabolism; D029721:Drosophila Proteins / Q000235:genetics* / Q000378:metabolism; D004331:Drosophila melanogaster / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism; D025461:Feedback, Physiological; D005247:Feeding Behavior / Q000502:physiology*; D005786:Gene Expression Regulation; D006706:Homeostasis; D009154:Mutation; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D009479:Neuropeptides / Q000235:genetics* / Q000378:metabolism; D020033:Protein Isoforms / Q000235:genetics / Q000378:metabolism; D015996:Survival Rate; D013569:Synapses / Q000378:metabolism
chemical_list: D000596:Amino Acids; D050483:Dopamine Plasma Membrane Transport Proteins; D029721:Drosophila Proteins; D009479:Neuropeptides; D020033:Protein Isoforms; C400215:neuropeptide F, Drosophila; D004298:Dopamine