Temperature is a ubiquitous environmental variable with major effects on physiology and behavior, and animals exhibit strong temperature-dependent orientation behaviors. However, the mechanisms that govern such orientation behaviors remain largely unknown. In this proposal, we propose to characterize the circuitry and the molecular mechanisms that guide this temperature-regulated behavior using molecular genetics in Drosophila.
The aims of this proposal are to:
Aim 1 : Identify the neurons governing thermotactic behavior. We will identify and assess the function of neurons involved in thermotaxis by using genetic approaches to ablate and inhibit the function of specific neurons.
Aim 2 : Examine the molecular properties of regulators of thermotaxis and test the hypothesis that candidate thermosensory neurons act by triggering repulsion from extreme temperatures.
Aim 3 : Investigate the molecular basis of differences in themosensory behavior and candidate thermal sensors.
Aim 4 : Identify additional regulators of themotaxis using a combination of RNAi-based and conventional genetic screens. The goal of this research is to understand the molecular mechanisms and neural circuits that control animal behavior, by focusing on the molecules and neuronal pathways involved in sensing and responding to environmental stimuli. Our long-term experimental goal is to obtain a molecular and cellular explanation of how Drosophila undergoes directed migration guided by temperature differentials. Our results should provide insight into how animals process sensory information in order to discriminate between subtle gradations in sensory input, a topic of relevanceto human perceptual disorders like agnosia resulting from stroke or dementia and hallucination associated with mental illness. Our work will also enhance understanding of the basic mechanisms of temperature sensation. Temperature perception is highly relevant to the perception of pain, and our studies should provide insights into how such somatosensory information is sensed and processed.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Program Projects (P01)
Project #
5P01NS044232-10
Application #
8305001
Study Section
Special Emphasis Panel (ZNS1)
Project Start
Project End
2013-07-31
Budget Start
2011-08-01
Budget End
2013-07-31
Support Year
10
Fiscal Year
2011
Total Cost
$288,341
Indirect Cost
Name
Brandeis University
Department
Type
DUNS #
616845814
City
Waltham
State
MA
Country
United States
Zip Code
02454
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Guo, Fang; Cerullo, Isadora; Chen, Xiao et al. (2014) PDF neuron firing phase-shifts key circadian activity neurons in Drosophila. Elife 3:
Li, Yue; Guo, Fang; Shen, James et al. (2014) PDF and cAMP enhance PER stability in Drosophila clock neurons. Proc Natl Acad Sci U S A 111:E1284-90
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Li, Yue; Rosbash, Michael (2013) Accelerated degradation of perS protein provides insight into light-mediated phase shifting. J Biol Rhythms 28:171-82
Ni, Lina; Bronk, Peter; Chang, Elaine C et al. (2013) A gustatory receptor paralogue controls rapid warmth avoidance in Drosophila. Nature 500:580-4
Shang, Yuhua; Donelson, Nathan C; Vecsey, Christopher G et al. (2013) Short neuropeptide F is a sleep-promoting inhibitory modulator. Neuron 80:171-83
Luo, Weifei; Li, Yue; Tang, Chih-Hang Anthony et al. (2012) CLOCK deubiquitylation by USP8 inhibits CLK/CYC transcription in Drosophila. Genes Dev 26:2536-49
Tang, Lamont S; Taylor, Adam L; Rinberg, Anatoly et al. (2012) Robustness of a rhythmic circuit to short- and long-term temperature changes. J Neurosci 32:10075-85

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