Model integration of circadian and sleep-wake driven contributions to rhythmic gene expression reveals novel regulatory principles
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1091667 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28445300.fastq.gz | Fastqsanger.gz | |||
| SRR28445400.fastq.gz | Fastqsanger.gz | |||
| SRR28445500.fastq.gz | Fastqsanger.gz | |||
| SRR28445301.fastq.gz | Fastqsanger.gz | |||
| SRR28445401.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 282 |
Similar Datasets
Project description:The timing and quality of sleep is regulated by circadian- and sleep–wake-driven processes. The core clock gene Bmal1 not only affects the circadian timing of sleep, but also the response to sleep deprivation (SD), which, in turn, causes long-term changes in cortical Bmal1 expression. We aimed at separating the circadian- and sleep–wake-driven contributions to BMAL1 binding to its target genes in the cerebral cortex by scheduling 6 SDs at 4 h intervals across the daily 12 h light/12 h dark cycle. We show that BMAL1 rhythmically bound its tissue-specific targets with tissue-specific dynamics, reaching peak binding 2 to 4 h later in the cortex than in the liver, while trough times did not differ. The SDs affected BMAL1 binding most significantly in the cortex, causing 80% of rhythmically bound regions to lose rhythmicity, suggesting BMAL1 binding has a prominent sleep–wake-driven component in this tissue. Analyses of the promoters of other core clock-genes indicate that BMAL1 binding to Bhlhe41 and Nr2d1 have a strong sleep–wake-driven component, while for Per2 two binding regions were identified one with circadian- and the other with sleep–wake-driven binding dynamics. Our results attest to a nonadditive interaction of time-of-day and time-spent-awake affecting the core molecular circadian circuitry. It further highlights that rhythms in gene expression in peripheral tissues are an emergent property of molecular interactions beyond that of the core molecular clock circuitry.
2025-11-27 | GSE299933 | GEO
Project description:We monitored gene expression in the liver of 10-12 week-old male C57BL/6J mice for 24 hours before and until 48 hours after the end of a single total sleep deprivation (SD) episode. The aim was to characterise the response to SD and recovery thereafter.
2024-07-01 | GSE262410 | GEO
Project description:The circadian clock drives daily changes of physiology, including sleep-wake cycles, by regulating transcription, protein abundance and function. Circadian phosphorylation controls cellular processes in peripheral organs, but little is known about its role in brain function and synaptic activity. We applied advanced quantitative phosphoproteomics to mouse forebrain synaptoneurosomes isolated across 24h, accurately quantifying almost 8,000 phosphopeptides. Remarkably, half of the synaptic phosphoproteins, including numerous kinases, had large-amplitude rhythms peaking at rest-activity and activity-rest transitions. Bioinformatic analyses revealed global temporal control of synaptic function via phosphorylation, including synaptic transmission, cytoskeleton reorganization and excitatory/inhibitory balance. Remarkably, sleep deprivation abolished 98% of all phosphorylation cycles in synaptoneurosomes, indicating that sleep-wake cycles rather than circadian signals are main drivers of synaptic phosphorylation, responding to both sleep and wake pressures.
2019-10-14 | PXD010697 | Pride
Project description:The sleep-wake cycle is determined by a circadian and a sleep homeostatic process. However, the molecular impact of these two processes and their interaction on different cell populations in the brain remain unknown. To fill this gap, we have profiled the single-cell transcriptome of adult fruit fly brains across the sleep-wake cycle and different circadian times. We show cell type-specific transcriptomic changes between sleep/wakefulness states, different levels of sleep drive, and varying circadian times, with glial cells displaying the largest variations. Furthermore, the cell types whose transcriptomic dynamics correlate with the sleep homeostat or circadian clock are largely non-overlapping, with the exception of glial cells. Diminishing the circadian clock only in glial cells impairs the homeostatic sleep rebound after sleep deprivation. These findings reveal a comprehensive picture of different effects of sleep homeostatic and circadian processes on different cell types and define glial cells as the interaction sites of these two processes to determine sleep-wake dynamics.
2023-11-29 | GSE221239 | GEO
Project description:Although the mammalian rest-activity cycle is controlled by a "master clock" in the suprachiasmatic nuclei (SCN) of the hypothalamus, it is unclear how firing of individual SCN neurons gates individual features of daily activity. Here, we demonstrate that a specific transcriptomically identified population of mouse VIP+ SCN neurons is active at the "wrong" time of the day -nighttime- when most SCN neurons are silent. Using chemogenetic and optogenetic strategies, we show that these neurons and their cellular clocks are necessary and sufficient to gate and time nighttime sleep, but have no effect upon daytime sleep. We propose mouse nighttime sleep, analogous to the human siesta, is a "hard-wired" property gated by specific neurons of the master clock to favor subsequent alertness prior to dawn (a circadian "wake maintenance zone"). Thus, the SCN is not simply a 24h metronome: specific populations sculpt critical features of the sleep-wake cycle.
2021-01-21 | GSE154038 | GEO
Project description:Sleep represents a fundamental biological necessity, yet the molecular mechanisms controlling this essential process remain largely unknown. Sleep disruption marks numerous pathological states, suggesting undiscovered molecular regulators govern this vital function. While studies have mapped gene expression during sleep, the master regulators that translate sleep pressure into sleep behavior have remained elusive. We demonstrate that Heat Shock Factor 1 (HSF1), previously characterized solely as a stress response transcription factor, serves as a critical molecular switch enabling sleep. HSF1's nuclear levels oscillate with sleep-wake cycles in mouse cortex and increase markedly during sleep deprivation. Systemic and brain-specific Hsf1 knockout mice display sleep disruption due to synaptic dysregulation, even as they accumulate normal sleep pressure. Nuclear HSF1 orchestrates a novel transcriptional program controlling synaptic organization, distinct from its canonical heat shock response. Single-nucleus RNA sequencing reveals that HSF1 deficiency triggers widespread dysregulation of synaptic genes across neuronal and glial populations. This mechanism shows evolutionary conservation, as Drosophila lacking the HSF1 ortholog display similar sleep phenotypes despite elevated sleep pressure. Our findings uncover an unexpected role for this classical stress factor and establish HSF1 as a molecular bridge linking sleep pressure to sleep behavior. These results suggest new therapeutic approaches for sleep disorders.
2025-12-05 | GSE283586 | GEO
Project description:Sleep represents a fundamental biological necessity, yet the molecular mechanisms controlling this essential process remain largely unknown. Sleep disruption marks numerous pathological states, suggesting undiscovered molecular regulators govern this vital function. While studies have mapped gene expression during sleep, the master regulators that translate sleep pressure into sleep behavior have remained elusive. We demonstrate that Heat Shock Factor 1 (HSF1), previously characterized solely as a stress response transcription factor, serves as a critical molecular switch enabling sleep. HSF1's nuclear levels oscillate with sleep-wake cycles in mouse cortex and increase markedly during sleep deprivation. Systemic and brain-specific Hsf1 knockout mice display sleep disruption due to synaptic dysregulation, even as they accumulate normal sleep pressure. Nuclear HSF1 orchestrates a novel transcriptional program controlling synaptic organization, distinct from its canonical heat shock response. Single-nucleus RNA sequencing reveals that HSF1 deficiency triggers widespread dysregulation of synaptic genes across neuronal and glial populations. This mechanism shows evolutionary conservation, as Drosophila lacking the HSF1 ortholog display similar sleep phenotypes despite elevated sleep pressure. Our findings uncover an unexpected role for this classical stress factor and establish HSF1 as a molecular bridge linking sleep pressure to sleep behavior. These results suggest new therapeutic approaches for sleep disorders.
2025-12-05 | GSE283583 | GEO
Project description:Sleep represents a fundamental biological necessity, yet the molecular mechanisms controlling this essential process remain largely unknown. Sleep disruption marks numerous pathological states, suggesting undiscovered molecular regulators govern this vital function. While studies have mapped gene expression during sleep, the master regulators that translate sleep pressure into sleep behavior have remained elusive. We demonstrate that Heat Shock Factor 1 (HSF1), previously characterized solely as a stress response transcription factor, serves as a critical molecular switch enabling sleep. HSF1's nuclear levels oscillate with sleep-wake cycles in mouse cortex and increase markedly during sleep deprivation. Systemic and brain-specific Hsf1 knockout mice display sleep disruption due to synaptic dysregulation, even as they accumulate normal sleep pressure. Nuclear HSF1 orchestrates a novel transcriptional program controlling synaptic organization, distinct from its canonical heat shock response. Single-nucleus RNA sequencing reveals that HSF1 deficiency triggers widespread dysregulation of synaptic genes across neuronal and glial populations. This mechanism shows evolutionary conservation, as Drosophila lacking the HSF1 ortholog display similar sleep phenotypes despite elevated sleep pressure. Our findings uncover an unexpected role for this classical stress factor and establish HSF1 as a molecular bridge linking sleep pressure to sleep behavior. These results suggest new therapeutic approaches for sleep disorders.
2025-12-05 | GSE283582 | GEO
Project description:The sleep–wake history contributes to rhythmic BMAL1 chromatin binding in the cerebral cortex but not in the liver
| PRJNA1277555 | ENA
Project description:Sleep-wake driven and circadian contributions to daily rhythms in gene expression and chromatin accessibility in the murine cortex
| PRJNA589315 | ENA