Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA258009 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Sleep dysfunction and stress susceptibility are co-morbid complex traits, which often precede and predispose patients to a variety of neuropsychiatric diseases. Here, we demonstrate multi-level organizations of genetic landscape, candidate genes, and molecular networks associated with 328 stress and sleep traits in a chronically stressed population of 338 (C57BL/6J×A/J) F2 mice. We constructed striatal gene co-expression networks, revealing functionally and cell-type-specific gene co-regulations important for stress and sleep. Using a composite ranking system, we identified network modules most relevant for 15 independent phenotypic categories, highlighting a mitochondria/synaptic module that links sleep and stress. The key network regulators of this module are overrepresented with genes implicated in neuropsychiatric diseases. Our work suggests the interplay between sleep, stress, and neuropathology emerge from genetic influences on gene expression and their collective organization through complex molecular networks, providing a framework to interrogate the mechanisms underlying sleep, stress susceptibility, and related neuropathology. Examination of genomic and transcriptomic networks in a random subset of 100 (B6xA/J)F2 mice modeling the natural spectrum of stress susceptibility.
2015-01-08 | E-GEOD-60312 | biostudies-arrayexpress
Project description:Sleep dysfunction and stress susceptibility are co-morbid complex traits, which often precede and predispose patients to a variety of neuropsychiatric diseases. Here, we demonstrate multi-level organizations of genetic landscape, candidate genes, and molecular networks associated with 328 stress and sleep traits in a chronically stressed population of 338 (C57BL/6J×A/J) F2 mice. We constructed striatal gene co-expression networks, revealing functionally and cell-type-specific gene co-regulations important for stress and sleep. Using a composite ranking system, we identified network modules most relevant for 15 independent phenotypic categories, highlighting a mitochondria/synaptic module that links sleep and stress. The key network regulators of this module are overrepresented with genes implicated in neuropsychiatric diseases. Our work suggests the interplay between sleep, stress, and neuropathology emerge from genetic influences on gene expression and their collective organization through complex molecular networks, providing a framework to interrogate the mechanisms underlying sleep, stress susceptibility, and related neuropathology.
2015-01-08 | GSE60312 | GEO
Project description:Sleep disruptions are among the most commonly-reported symptoms across neurodevelopmental disorders (NDDs), but mechanisms linking brain development to normal sleep are largely unknown. From a Drosophila screen of human NDD-associated risk genes, we identified the chromatin remodeler Imitation SWItch/SNF (ISWI) to be required for adult fly sleep. To better understand the mechanisms by which ISWI regulates sleep, we performed RNA-Seq analysis on mid-3rd instar larval central nervous systems (central brain + ventral nerve cord) in the setting of pan-neuronal ISWI knockdown (elav-GAL4>UAS-ISWI RNAi) compared to controls (elav-GAL4;+). We chose mid-3rd instar because temporal mapping revealed ISWI knockdown during this pre-adult developmental stage led to adult fly sleep deficits.
2020-11-02 | GSE160591 | GEO
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>
2023-03-18 | MTBLS3318 | MetaboLights
Project description:We used a systems genetics approach in the BXD genetic reference population of mice and assembled a comprehensive experimental knowledge base comprising a deep ‘sleep-wake’ phenome, central and peripheral transcriptomes, and plasma metabolome data, collected under undisturbed baseline conditions and after sleep deprivation.
2018-06-26 | GSE114845 | GEO
Project description:Sleep and affective behaviors are highly interrelated phenotypes, commonly altered in a variety of neuropsychiatric diseases, including major depressive disorder (MDD). To understand the transcriptomic organization underlying sleep and affective function, we studied a population of (C57BL/6J x 129S1/SvImJ) F2 mice by measuring 283 affective and sleep phenotypes and profiling gene expression across four brain regions, including the frontal cortex, hippocampus, thalamus, and hypothalamus. We identified converging molecular bases for sleep and affective phenotypes at both the single-gene and gene-network levels. Utilizing publicly available transcriptomic datasets collected from sleep-deprived mice and major depressive disorder (MDD) patients, we identified three cortical gene networks altered by sleep/wake changes and depression. The network-level actions of sleep loss and depression were opposite to each other, providing a mechanistic basis for the sleep disruptions commonly observed in depression as well as the reported acute antidepressant effects of sleep deprivation. We highlight one particular network composed of circadian rhythm regulators and neuronal activity-dependent immediate-early genes. The key upstream driver of this network, Arc, may act as a nexus linking sleep and depression. Our data provide mechanistic insights into the role of sleep in affective function and MDD.
2018-12-21 | GSE109112 | GEO
Project description:Due to the broad climate adaptation of perennial trees, phenological traits (e.g. chilling requirement-CR, bloom date-BD) exhibit complex inheritance patterns. Conceptually, these are adaptive responses to abiotic stress. As production depends on traits like CR, breeders have developed varieties that are phenotypically/genotypically matched to particular geographic/temperature zones. These genotypes are ideal for study of gene networks governing these climate-critical traits. Using genetic approaches, genome-wide association analyses, functional and comparative genomics in fruit and forest trees, we identified a foundational network of genetic activity (phenylpropanoid pathway) linking winter cold stress response to control of the endodormancy-ecodormancy transition (EET) and seed stratification. Our goal is to examine during endodormancy the allelic effects of genes controlling the production of stress related metabolic intermediates that regulate seed stratification, thus linking these two cold temperature responses. Our objective is to use a transcriptome sequencing approach to characterize genotypic effects on the phenylpropanoid gene network transcriptome during endodormancy and the EET. These adaptive genes and gene networks will be targets for knowledge based breeding strategies of fruit and forest trees to sustain and improve these resources to meet the challenges of rapid environmental change
2020-03-23 | GSE138792 | GEO
Project description:Systems genetics of sleep regulation
| PRJNA472805 | ENA
Project description:Insomnia is an economic burden and public health problem. This study aimed to explore potential biological pathways and protein networks for insomnia characterized by wakefulness after sleep. Proteomics analysis was performed in the insomnia group with wakefulness and the control group. The differentially expressed proteins (DEPs) were enriched, then hub proteins were identified by protein-protein interaction (PPI) network and verified by parallel reaction monitoring (PRM). Compared with the control group, the sleep time and efficiency of insomnia patients were decreased, awakening time and numbers after sleep onset were significantly increased (P < 0.001). The results of proteomic sequencing found 68 DEPs in serum under 1.2-fold changed standard. These DEPs were significantly enriched in humoral immune response, complement and coagulation cascades, cholesterol metabolism. Through PPI network, we identified 10 proteins with the highest connectivity as hub proteins. Among them, differential expression of 9 proteins was verified by PRM.We identified the hub proteins and molecular mechanisms of insomnia patients characterized by wakefulness after sleep. It provided potential molecular targets for the clinical diagnosis and treatment of these patients, and indicated the immune and metabolic systems may be closely related to insomnia characterized by wakefulness after sleep.
2021-09-09 | PXD023246 | Pride
Project description:Sleep is deeply involved in neuroimmune regulation, while the mechanism is yet to be elucidated. Experimental manipulation of sleep duration provides a reliable measure for evaluating how sleep regulates innate immunity. Here we report a modified sleep deprivation paradigm (SD) that can constantly awaken the mice with more than 95% efficiency, and investigate the effects of prolonged sleep deprivation on mice's immune systems.
2023-11-27 | GSE213497 | GEO