Disruption of Circadian Transcriptome in Lung by Acute Sleep Deprivation
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ABSTRACT:
PROVIDER: PRJNA700534 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13649900_1.fastq.gz | Fastqsanger.gz | |||
| SRR13649900_2.fastq.gz | Fastqsanger.gz | |||
| SRR13649901_1.fastq.gz | Fastqsanger.gz | |||
| SRR13649901_2.fastq.gz | Fastqsanger.gz | |||
| SRR13649902_1.fastq.gz | Fastqsanger.gz |
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Project description:Inadequate sleep prevails in modern society and it impairs the circadian transcriptome. However, whether acute sleep deprivation has impact on the circadian rhythms is not clear. Here, we show that in mouse lung, a 10-hour acute sleep deprivation can alter the circadian expression of approximally 3,000 genes. We found that circadian rhythm disappears in genes related to metabolism and signaling pathways regulating protein phosphorylation after acute sleep deprivation, while the core circadian regulators do not change much in rhythmicity. Importantly, the strong positive correlation between mean expression and amplitude (E-A correlation) of cycling genes has been validated in both control and sleep deprivation conditions, supporting the energetic cost optimization model of circadian gene expression. Thus, we reveal that acute sleep deprivation leads to a profound change in the circadian gene transcription that influences the biological functions in lung.
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Project description:Purpose: To comprehensively identify the gene expression changes that occur after acute sleep deprivation. Method: We performed total RNA sequencing after 5hours of sleep deprivation. Results: Using total RNA-sequencing, we show that acute sleep deprivation causes dramatic gene expression changes in the mouse hippocampus. Conclusion: This study provides insight into the biological impact of acute sleep deprivation.
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Project description:Despite an established link between sleep deprivation and epigenetic processes in humans, it remains unclear to what extent sleep deprivation modulates DNA methylation. We performed a within subject randomized blinded study with 16 healthy subjects to examine the effect of one night of total acute sleep deprivation (TSD) on the genome wide methylation profile in blood compared to normal sleep. Genome-wide differences in methylation between both conditions were assessed by applying a paired regression model that corrected for monocyte subpopulations (neutrophil/leukocyte ratio). Additionally, the correlations between the methylation of genes detected to be modulated by TSD and gene expression were examined in a separate, publicly available cohort of ten healthy male donors (E-GEOD-49065). Sleep deprivation significantly affected the DNA methylation profile both independently and in dependency of shifts in monocyte composition. Our study detected differential methylation of 269 probes. Notably, one CpG site was located 69bp upstream of ING5, which has been shown to be differentially expressed following sleep deprivation. Gene set enrichment analysis detected the Notch and Wnt signaling pathways to be enriched among the differentially methylated genes. These results provide evidence that total acute sleep deprivation alters the methylation profile in healthy human subjects. This is, to our knowledge, the first study that systematically investigated the impact of total acute sleep deprivation on genome-wide DNA methylation profiles in blood and related the epigenomic findings to the expression data.
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Project description:To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation (SD). Blood draws every 4 hours during a 3-day study: 24-hour normal baseline, 38 hours of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-hr psychomotor vigilance test (PVT) assessment when awake. Fourteen subjects who were previously identified as behaviourally resistant (n=7) or sensitive (n=7) to SD by PVT. Intervention consisted of 38 hours continuous wakefulness. We found 4,481 unique genes with a significant 24-hour diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] <5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of SD (FDR<5%). The main change with SD was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviourally resistant subjects than sensitive subjects, at any given p-value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Individual differences in behavioural effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity.
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Project description:To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation (SD). Blood draws every 4 hours during a 3-day study: 24-hour normal baseline, 38 hours of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-hr psychomotor vigilance test (PVT) assessment when awake. Fourteen subjects who were previously identified as behaviourally resistant (n=7) or sensitive (n=7) to SD by PVT. Intervention consisted of 38 hours continuous wakefulness. We found 4,481 unique genes with a significant 24-hour diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] <5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of SD (FDR<5%). The main change with SD was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviourally resistant subjects than sensitive subjects, at any given p-value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Individual differences in behavioural effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity. Blood draws were done every 4 hours during a 3-day (+1 baseline day) study: 24-hour normal baseline (6 time points: day 1 8hr, 12hr, 16hr, 20hr, day 2 0hr, 4hr), 38 hours of continuous wakefulness (10 time points: day 2 8hr, 12hr, 16hr, 20hr, day 3 0hr, 4hr, 8hr, 12hr, 16hr, 20hr) and subsequent recovery sleep (3 time points: day 4 0hr, 4hr, 8hr), for a total of 19 time-points per subject, with every 2-hr psychomotor vigilance test (PVT) assessment when awake. The missing/failed samples were as following: Resistant subjects (total 10 samples): BH006 day 2 20hr, 12hr, BH003 day 2 12hr, 4hr, BH003 day 3 4hr, BH008 day 4 0hr, BH008 day 1 16hr, BH008 day 3 16hr 20hr, BH010 day 4 0hr; Sensitive subjects (total 7 samples): BH004 day 2 12hr and 1 more missing sample, BH026 day 2 4hr, BH007 day 2 20hr and 1 more missing sample, BH016 day 2 4hr, BH015 day 3 0hr.
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