Nutritional geometry framework on sleep in Drosophila
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ABSTRACT:
PROVIDER: PRJNA778774 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16868638_1.fastq.gz | Fastqsanger.gz | |||
| SRR16868638_2.fastq.gz | Fastqsanger.gz | |||
| SRR16868639_1.fastq.gz | Fastqsanger.gz | |||
| SRR16868639_2.fastq.gz | Fastqsanger.gz | |||
| SRR16868640_1.fastq.gz | Fastqsanger.gz |
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Project description:Sleep is a fundamental physiological function and is essential for all animals, including humans. Sleep has been reported to be affected by diet compositions including protein (P) and carbohydrates (C), but there has not been a systematic investigation of the effect of dietary macronutrient balance on sleep. Here, we used the nutritional geometry framework (NGF) to explore the interactive effects on sleep of protein (P) and carbohydrate (C) in the model organism Drosophila. Our results showed that the combination of low protein and moderate carbohydrate prolonged sleep time and sleep quality, with fewer sleep episodes and longer sleep duration. We further found that the effects of macronutrients on sleep mirrored levels of haemolymph glucose and whole-body glycogen. Moreover, transcriptome analyses revealed that high protein, low carbohydrate diet elevated the gene expression of amino acid metabolic pathways when compared to a diet lacking protein, with the glycine, serine, threonine metabolism pathway being most strongly regulated. However, sleep was not decreased in flies fed on a protein-deficient diet with added glycine, serine and threonine. In summary, our results demonstrate that sleep is affected by the balance of protein and carbohydrates in the diet and that reduced protein coupled with moderate carbohydrate promote sleep duration and quality.
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Project description:<p>Chronic sleep loss profoundly impacts metabolic health and shortens lifespan, but studies of the mechanisms involved have focused largely on acute sleep deprivation. To identify metabolic consequences of chronically reduced sleep, we conducted unbiased metabolomics on heads of three adult Drosophila short-sleeping mutants with very different mechanisms of sleep loss: fumin (fmn), redeye (rye), and sleepless (sss). Common features included elevated ornithine and polyamines, with lipid, acyl-carnitine, and TCA cycle changes suggesting mitochondrial dysfunction. Studies of excretion demonstrate inefficient nitrogen elimination in adult sleep mutants, likely contributing to their polyamine accumulation. Increasing levels of polyamines, particularly putrescine, promote sleep in control flies but poison sleep mutants. This parallels the broadly enhanced toxicity of high dietary nitrogen load from protein in chronically sleep-restricted Drosophila, including both sleep mutants and flies with hyper-activated wake-promoting neurons. Together, our results implicate nitrogen stress as a novel mechanism linking chronic sleep loss to adverse health outcomes-and perhaps for linking food and sleep homeostasis at the cellular level in healthy organisms.</p>
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Project description:Numerous studies show dietary carbohydrates (C) affect the sensation of sweetness. However, protein (P) is one of the most critical macronutrients in the diet as well. It is still unclear how carbohydrates and proteins interact to influence sweet taste sensitivity. Here, we use the nutritional geometry framework (NGF) to tackle this problem in Drosophila melanogaster. Our results showed that the combination of high protein and low carbohydrates caused higher taste responses to sucrose stimuli in both sexes. Additionally, transcriptome analysis revealed that the gene expression of glycine, serine, and threonine pathway in the high-protein, low-carbohydrate diet was significantly upregulated, compared to a diet with low protein, and high carbohydrate. We confirmed that serine and threonine supplementation in the high-carbohydrate, low-protein diet enhanced the sucrose sensitivity of flies. Our results demonstrate that sucrose taste sensitivity is affected by the dietary balance of protein and carbohydrates possibly mediated by the change in serine, and threonine. The high protein, low carbohydrate diets enhanced sucrose taste sensitivity.
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Project description:To gain insight into the dynamic molecular processes that are altered during prolonged wakefulness and during sleep. We performed an RNA expression profiling study examining temporal changes in the brain of Drosophila in relationship to the duration of prior sleep or wakefulness. Our experimental design allowed us to determine whether genes identified as differentially regulated between sleep and wakefulness were up- or down-regulated in these states. Because stimulation of the experimental animal during the normal sleep period is used to prolong wakefulness in most experimental paradigms, the interpretation of the effects of prolonged wakefulness is confounded by the effect of the perturbation stimulus itself on the animal’s biology. We controlled for this effect in our experimental paradigm by examining gene expression changes in response to identical stimulation but during the animal’s normal wakefulness. The design of our study also allowed us to control for circadian variation in gene expression, since we compared sleeping and sleep deprived flies at the same diurnal time. Keywords: sleep deprivation, time course, stress response
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Project description:Sleep is a conserved physiological process, and sleep loss typically imposes negative effects on animal health. However, natural short sleepers, who sleep less without the usual negative effects of sleep deprivation, exist in the human population. One example are individuals that possess rare genetic mutations in the human dec2 gene; these individuals sleep on average ~6hrs/day rather than the typical 8hrs/day. Like many natural short sleepers, humans harboring the dec2P384R mutation do not exhibit any obvious adverse phenotypes typically associated with sleep loss, suggesting that these individuals may require less total sleep/day to achieve the same physiological outcomes. Potentially, the dec2P384R mutation could activate compensatory mechanisms that allow these individuals to thrive with less sleep. To test this directly, we used a dec2P384R short sleep Drosophila model to understand the effects of the dec2P384R mutation on animal health and dissect the genetic mechanisms that might drive these physiological changes. We found that expression of the mammalian dec2P384R mutation in fly sleep neurons was sufficient to mimic the short sleep phenotype observed in mammals. Remarkably, dec2P384R lived significantly longer with improved health and memory despite having a short sleep phenotype. The improved physiological effects in dec2P384R mutants were enabled, in part, by enhanced mitochondrial fitness and upregulation of multiple stress response pathways. Moreover, we provide evidence that the improved health in dec2P384R mutants may also contribute to the short sleep phenotype, and this may extend to other pro-longevity mutants.
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Project description:Genome-wide profiling of rhythmic gene expression has offered new avenues for studying the contribution of circadian clock to diverse biological processes. Sleep has been considered one of the most important physiological processes that are regulated by the circadian clock, however, the effects of chronic sleep loss on rhythmic gene expression remain poorly understood. In the present study, we exploited Drosophila sleep mutants insomniac1 (inc1) and wide awakeD2 (wakeD2) as models for chronic sleep loss. We profiled the transcriptomes of heads collected from 4-week-old wild type flies, inc1 and wakeD2 at timepoints around the clock. Analysis of gene oscillation revealed a substantial loss of rhythmicity in inc1 and wakeD2 compared to wild type flies, with most of the affected genes common to both mutants. The disruption of gene oscillation was not due to changes in average gene expression levels. We also identified a subset of genes whose loss of rhythmicity was shared among animals with chronic sleep loss and old flies, suggesting a contribution of aging to chronic, sleep-loss-induced disruption of gene oscillation.
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Project description:Transcriptomic DN3 clock neuron subtypes regulate Drosophila sleep
| PRJNA1155627 | ENA