Motor Control in a Drosophila Taste Circuit

Department of Molecular and Cell Biology and Helen Wills Neuroscience Institute, 291 Life Sciences Addition, University of California, Berkeley, Berkeley, CA 94720, USA.
Neuron (Impact Factor: 15.05). 03/2009; 61(3):373-84. DOI: 10.1016/j.neuron.2008.12.033
Source: PubMed

ABSTRACT Tastes elicit innate behaviors critical for directing animals to ingest nutritious substances and reject toxic compounds, but the neural basis of these behaviors is not understood. Here, we use a neural silencing screen to identify neurons required for a simple Drosophila taste behavior and characterize a neural population that controls a specific subprogram of this behavior. By silencing and activating subsets of the defined cell population, we identify the neurons involved in the taste behavior as a pair of motor neurons located in the subesophageal ganglion (SOG). The motor neurons are activated by sugar stimulation of gustatory neurons and inhibited by bitter compounds; however, experiments utilizing split-GFP detect no direct connections between the motor neurons and primary sensory neurons, indicating that further study will be necessary to elucidate the circuitry bridging these populations. Combined, these results provide a general strategy and a valuable starting point for future taste circuit analysis.

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    • "Promoter-driven Gal80 Gal4 and Gal80 expression is driven by two different enhancers, in cells of overlap, Gal80 inhibits Gal4 activity (Keene et al. 2004; Clyne and Miesenböck 2008 Heat-shock FLP-mediated Gal80 Flip-Out Tub p >Gal80>, tubulin-promoter-driven Gal80 flanked by FRT sites. Gal80 can be flipped out by hs-FLP (Gordon and Scott 2009) Enhancer-trap FLP-mediated Flip-In and Flip-Out Gal80 (FINGR) "
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    ABSTRACT: Understanding behavior requires unraveling the mysteries of neurons, glia, and their extensive connectivity. Drosophila has emerged as an excellent organism for studying the neural basis of behavior. This can be largely attributed to the extensive effort of the fly community to develop numerous sophisticated genetic tools for visualizing, mapping, and manipulating behavioral circuits. Here, we attempt to highlight some of the new reagents, techniques and approaches available for dissecting behavioral circuits in Drosophila. We focus on detailing intersectional strategies such as the Flippase-induced intersectional Gal80/Gal4 repression (FINGR), because of the tremendous potential they possess for mapping the minimal number of cells required for a particular behavior. The logic and strategies outlined in this review should have broad applications for other genetic model organisms.
    Journal of Comparative Physiology 04/2015; 201(9). DOI:10.1007/s00359-015-1010-y · 2.04 Impact Factor
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    • "The fruit fly assesses the quality of potential food sources using gustatory neurons that detect sweet and bitter compounds and drive acceptance and rejection, respectively (Thorne et al., 2004; Wang et al., 2004). In addition, motor neurons controlling feeding subprograms for proboscis extension and ingestion have been described (Gordon and Scott, 2009; Manzo et al., 2012; Rajashekhar and Singh, 1994; Tissot et al., 1998). Only one taste-responsive interneuron has been characterized to date: a putative feeding-command neuron that is activated by sugar and promotes feeding (Flood et al., 2013). "
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    ABSTRACT: Feeding is dynamically regulated by the palatability of the food source and the physiological needs of the animal. How consumption is controlled by external sensory cues and internal metabolic state remains under intense investigation. Here, we identify four GABAergic interneurons in the Drosophila brain that establish a central feeding threshold which is required to inhibit consumption. Inactivation of these cells results in indiscriminate and excessive intake of all compounds, independent of taste quality or nutritional state. Conversely, acute activation of these neurons suppresses consumption of water and nutrients. The output from these neurons is required to gate activity in motor neurons that control meal initiation and consumption. Thus, our study reveals a layer of inhibitory control in feeding circuits that is required to suppress a latent state of unrestricted and nonselective consumption.
    Neuron 07/2014; 83(1):164-77. DOI:10.1016/j.neuron.2014.05.006 · 15.05 Impact Factor
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    • "In this technique, two different cell populations are made to express individual split GFP components (GFP11 and GFP1-10), which reconstitute a functional GFP molecule if these cells come into close contact with one another (Feinberg et al., 2008; Gordon and Scott, 2009). GRASP is typically used with the LexA-LexAop and GAL4-upstream activating sequence (UAS) systems (Gordon and Scott, 2009). We also made a transgenic fly in which we placed the GFP11 fragment downstream of a QUAS element in order to adapt the technique for use with the QF-QUAS system (Potter et al., 2010). "
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    ABSTRACT: Though much is known about the cellular and molecular components of the circadian clock, output pathways that couple clock cells to overt behaviors have not been identified. We conducted a screen for circadian-relevant neurons in the Drosophila brain and report here that cells of the pars intercerebralis (PI), a functional homolog of the mammalian hypothalamus, comprise an important component of the circadian output pathway for rest:activity rhythms. GFP reconstitution across synaptic partners (GRASP) analysis demonstrates that PI cells are connected to the clock through a polysynaptic circuit extending from pacemaker cells to PI neurons. Molecular profiling of relevant PI cells identified the corticotropin-releasing factor (CRF) homolog, DH44, as a circadian output molecule that is specifically expressed by PI neurons and is required for normal rest:activity rhythms. Notably, selective activation or ablation of just six DH44+ PI cells causes arrhythmicity. These findings delineate a circuit through which clock cells can modulate locomotor rhythms.
    Cell 04/2014; 157(3):689-701. DOI:10.1016/j.cell.2014.02.024 · 32.24 Impact Factor
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