Characterization of<b><i>Drosophila Tyramine β-Hydroxylase</i></b>Gene and Isolation of Mutant Flies Lacking Octopamine

Monastirioti, Maria; Linn, Charles E.; White, K. Andrew

doi:10.1523/jneurosci.16-12-03900.1996

Cited by 365 publications

(458 citation statements)

References 45 publications

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“…TβH catalyzes the rate-limiting step of octopamine biosynthesis in which tyramine is converted to octopamine (32). It is therefore possible that the lack of starvation-induced hyperactivity in TβH M18 mutants may result from increased tyramine level rather than from lack of octopamine.…”

Section: Significancementioning

confidence: 99%

Octopamine mediates starvation-induced hyperactivity in adult Drosophila

Yang

Zhang

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

171

180

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Starved animals often exhibit elevated locomotion, which has been speculated to partly resemble foraging behavior and facilitate food acquisition and energy intake. Despite its importance, the neural mechanism underlying this behavior remains unknown in any species. In this study we confirmed and extended previous findings that starvation induced locomotor activity in adult fruit flies Drosophila melanogaster. We also showed that starvationinduced hyperactivity was directed toward the localization and acquisition of food sources, because it could be suppressed upon the detection of food cues via both central nutrient-sensing and peripheral sweet-sensing mechanisms, via induction of food ingestion. We further found that octopamine, the insect counterpart of vertebrate norepinephrine, as well as the neurons expressing octopamine, were both necessary and sufficient for starvationinduced hyperactivity. Octopamine was not required for starvation-induced changes in feeding behaviors, suggesting independent regulations of energy intake behaviors upon starvation. Taken together, our results establish a quantitative behavioral paradigm to investigate the regulation of energy homeostasis by the CNS and identify a conserved neural substrate that links organismal metabolic state to a specific behavioral output.T he CNS plays an essential role in energy homeostasis (1). It actively monitors changes in the internal energy state and modulates an array of physiological and behavioral responses to enable energy homeostasis. Foraging behavior is critical for the localization and acquisition of food supply and hence energy homeostasis. It has been extensively documented both in ethological settings (2, 3) and under well-controlled laboratory conditions (4). Laboratory rodents with limited food access exhibit stereotypic food anticipatory activity (FAA) several hours before the mealtime, which is characterized by a steady increase in locomotion and other appetitive behaviors (5). The neural substrate that drives FAA still remains elusive (5, 6). Notably, the regulation of FAA seems to be dissociable from that of feeding behavior (7,8). These results hint at the presence of an independent and somewhat discrete regulatory mechanism of foraging behavior.Foraging behavior has also been extensively studied in invertebrate species such as the roundworm Caenorhabditis elegans (9) and fruit flies Drosophila melanogaster (10). Roundworm populations exhibit two naturally emerged foraging patterns: "solitary" worms disperse across the bacterial lawn, and "social" worms aggregate along the food edge and form clumps (9). This behavioral dimorphism is controlled by natural variations of the npr-1 (neuropeptide receptor resemblance) gene that encodes a receptor homologous to the receptor family of orexigenic neuropeptide Y in mammals (9). A comparable scenario has also been identified in larval fruit flies (10), with two distinct forms of foraging present in nature: "rover" and "sitter." On food sources, sitter but not rover reduces moving speed ...

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Section: Significancementioning

confidence: 99%

Octopamine mediates starvation-induced hyperactivity in adult Drosophila

Yang

Zhang

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

171

180

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“…This follicle rupture also relies on proteolytic enzymes, like matrix metalloproteinase 2 (Mmp2), which is specifically expressed in the posterior follicle cells of stage-14 egg chambers (9). Mmp2 activation is stimulated by the monoamine octopamine (OA), which is equivalent to norepinephrine in mammals and is essential for ovulation (10,11). OA binds to its receptor Octopamine receptor in mushroom body (Oamb) in mature follicle cells to induce an intracellular calcium rise, Mmp2 activation, and follicle rupture (12).…”

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confidence: 99%

Steroid signaling in mature follicles is important for Drosophila ovulation

Knapp

Sun

2017

Proc. Natl. Acad. Sci. U.S.A.

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Although ecdysteroid signaling regulates multiple steps in oogenesis, it is not known whether it regulates Drosophila ovulation, a process involving a matrix metalloproteinase-dependent follicle rupture. In this study, we demonstrated that ecdysteroid signaling is operating in mature follicle cells to control ovulation. Moreover, knocking down shade (shd), encoding the monooxygenase that converts ecdysone (E) to the more active 20-hydroxyecdysone (20E), specifically in mature follicle cells, blocked follicle rupture, which was rescued by ectopic expression of shd or exogenous 20E. In addition, disruption of the Ecdysone receptor (EcR) in mature follicle cells mimicked shd-knockdown defects, which were reversed by ectopic expression of EcR.B2 but not by EcR.A or EcR.B1 isoforms. Furthermore, we showed that ecdysteroid signaling is essential for the proper activation of matrix metalloproteinase 2 (Mmp2) for follicle rupture. Our data strongly suggest that 20E produced in follicle cells before ovulation activates EcR.B2 to prime mature follicles to be responsive to neuronal ovulatory stimuli, thus providing mechanistic insights into steroid signaling in Drosophila ovulation.steroid signaling | ecdysone | ovulation | Shade | EcR isoforms

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“…10), including Drosophila female fertility. Flies that lack a functional octopamine receptor or cannot synthesize octopamine due to a null allele of tyramine ␤-hydroxylase (T␤h) 2 show a complete egg retention phenotype (11)(12)(13). The sterility of T␤h null females is due to a defect in ovulation, which can be rescued by octopamine feeding or by driving the ectopic expression of a T␤h transgene in several driver lines that show overlapping expression in the thoracic tip of the CNS (12,13).…”

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confidence: 99%

Two Functional but Noncomplementing Drosophila Tyrosine Decarboxylase Genes

Cole

Carney

McClung³

et al. 2005

Journal of Biological Chemistry

305

177

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The trace biogenic amine tyramine is present in the nervous systems of animals ranging in complexity from nematodes to mammals. Tyramine is synthesized from tyrosine by the enzyme tyrosine decarboxylase (TDC), a member of the aromatic amino acid family, but this enzyme has not been identified in Drosophila or in higher animals. To further clarify the roles of tyramine and its metabolite octopamine, we have cloned two TDC genes from Drosophila melanogaster, dTdc1 and dTdc2. Although both gene products have TDC activity in vivo, dTdc1 is expressed nonneurally, whereas dTdc2 is expressed neurally. Flies with a mutation in dTdc2 lack neural tyramine and octopamine and are female sterile due to egg retention. Although other Drosophila mutants that lack octopamine retain eggs completely within the ovaries, dTdc2 mutants release eggs into the oviducts but are unable to deposit them. This specific sterility phenotype can be partially rescued by driving the expression of dTdc2 in a dTdc2-specific pattern, whereas driving the expression of dTdc1 in the same pattern results in a complete rescue. The disparity in rescue efficiencies between the ectopically expressed Tdc genes may reflect the differential activities of these gene products. The egg retention phenotype of the dTdc2 mutant and the phenotypes associated with ectopic dTdc expression contribute to a model in which octopamine and tyramine have distinct and separable neural activities.Tyramine, octopamine, and other "trace" biogenic amines are found in most organisms, including bacteria, fungi, and plants, and in animals ranging in complexity from nematodes to mammals. Despite their wide distribution, the biological roles of trace amines are poorly understood. In vertebrates, trace amines are present in low levels and can displace classical biogenic amines from their stores and stimulate outward neurotransmitter efflux from biogenic amine transporters (1). Although there are currently no data to suggest that there are dedicated synapses for trace amines in the brain, the recent discovery of G-protein-coupled receptors that are selectively Additionally, tyramine affects chloride permeability in the Drosophila Malpighian tubule (7), relaxation of muscle tone in the locust oviduct (8), and behavioral responses to cocaine in Drosophila (9).Octopamine in invertebrates is often considered to be the functional homolog of vertebrate norepinephrine and is involved in a diverse range of physiological processes (reviewed in Ref. 10), including Drosophila female fertility. Flies that lack a functional octopamine receptor or cannot synthesize octopamine due to a null allele of tyramine ␤-hydroxylase (T␤h) 2 show a complete egg retention phenotype (11-13). The sterility of T␤h null females is due to a defect in ovulation, which can be rescued by octopamine feeding or by driving the ectopic expression of a T␤h transgene in several driver lines that show overlapping expression in the thoracic tip of the CNS (12, 13).The first step in octopamine biosynthesis is catalyzed by tyrosine...

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Characterization ofDrosophila Tyramine β-HydroxylaseGene and Isolation of Mutant Flies Lacking Octopamine

Cited by 365 publications

References 45 publications

Octopamine mediates starvation-induced hyperactivity in adult Drosophila

Octopamine mediates starvation-induced hyperactivity in adult Drosophila

Steroid signaling in mature follicles is important for Drosophila ovulation

Two Functional but Noncomplementing Drosophila Tyrosine Decarboxylase Genes

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