Drosophila insulin-like peptide 2 mediates dietary regulation of sleep intensity

Autor: Alex C. Keene, Elizabeth B. Brown, Kreesha D. Shah, Benjamin Kottler, Richard Faville
Jazyk: angličtina
Rok vydání: 2019
Předmět:
Cancer Research
Physiology
QH426-470
0302 clinical medicine
Mathematical and Statistical Techniques
Animal Cells
Medicine and Health Sciences
Drosophila Proteins
Insulin
Homeostasis
Genetics (clinical)
Starvation
2. Zero hunger
Neurons
0303 health sciences
biology
Drosophila Melanogaster
Statistics
Eukaryota
Animal Models
Sleep in non-human animals
Insects
Neurology
Experimental Organism Systems
Physical Sciences
Drosophila
Analysis of variance
medicine.symptom
Drosophila melanogaster
Cellular Types
Research Article
Arthropoda
Period (gene)
Research and Analysis Methods
03 medical and health sciences
Model Organisms
medicine
Biological neural network
Genetics
Animals
Statistical Methods
Molecular Biology
Ecology
Evolution
Behavior and Systematics
030304 developmental biology
Nutrition
Analysis of Variance
Neuropeptides
Malnutrition
Organisms
Biology and Life Sciences
Cell Biology
biology.organism_classification
Invertebrates
Diet
Insulin receptor
Sleep deprivation
Cellular Neuroscience
biology.protein
Animal Studies
Sleep Deprivation
Sleep
Physiological Processes
Neuroscience
030217 neurology & neurosurgery
Relaxin/insulin-like family peptide receptor 2
Mathematics
Zdroj: PLoS Genetics
PLoS Genetics, Vol 16, Iss 3, p e1008270 (2020)
DOI: 10.1101/681551
Popis: Sleep is a nearly universal behavior that is regulated by diverse environmental stimuli and physiological states. A defining feature of sleep is a homeostatic rebound following deprivation, where animals compensate for lost sleep by increasing sleep duration and/or sleep depth. The fruit fly, Drosophila melanogaster, exhibits robust recovery sleep following deprivation and represents a powerful model to study neural circuits regulating sleep homeostasis. Numerous neuronal populations have been identified in modulating sleep homeostasis as well as depth, raising the possibility that the duration and quality of recovery sleep is dependent on the environmental or physiological processes that induce sleep deprivation. Here, we find that unlike most pharmacological and environmental manipulations commonly used to restrict sleep, starvation potently induces sleep loss without a subsequent rebound in sleep duration or depth. Both starvation and a sucrose-only diet result in increased sleep depth, suggesting that dietary protein is essential for normal sleep depth and homeostasis. Finally, we find that Drosophila insulin like peptide 2 (Dilp2) is acutely required for starvation-induced changes in sleep depth without regulating the duration of sleep. Flies lacking Dilp2 exhibit a compensatory sleep rebound following starvation-induced sleep deprivation, suggesting Dilp2 promotes resiliency to sleep loss. Together, these findings reveal innate resilience to starvation-induced sleep loss and identify distinct mechanisms that underlie starvation-induced changes in sleep duration and depth.
Author summary Sleep is nearly universal throughout the animal kingdom and homeostatic regulation represents a defining feature of sleep, where animals compensate for lost sleep by increasing sleep over subsequent time periods. Despite the robustness of this feature, the neural mechanisms regulating recovery from different types of sleep deprivation are not fully understood. Fruit flies provide a powerful model for investigating the genetic regulation of sleep, and like mammals, display robust recovery sleep following deprivation. Here, we find that unlike most stimuli that suppress sleep, sleep deprivation by starvation does not require a homeostatic rebound. These findings are likely due to flies engaging in deeper sleep during the period of partial sleep deprivation, suggesting a natural resilience to starvation-induced sleep loss. This unique resilience to starvation-induced sleep loss is dependent on Drosophila insulin-like peptide 2, revealing a critical role for insulin signaling in regulating interactions between diet and sleep homeostasis.
Databáze: OpenAIRE
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