The phase-shifting effect of bright light exposure on circadian rhythmicity in the human transcriptome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA506081 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Eleven healthy human subjects were enrolled in a 6-day simulated shift work protocol. Blood samples were collected during the two 24-hour measurement periods. Blood samples were collected every 4 hours during both measurement periods. Subjects entered the lab on Day 1. At the start of Day 2, the first 24-hour measurement period was started. Subjects slept according to their habitual sleep/wake schedule, followed by a 16-hour constant posture procedure. On days 3-6, the sleep period was delayed by 10 hours. Participants in the control group were exposed to dim light throughout the waking periods; participants in the bright group were exposed to bright light (~6,000lux) for 8 hours during the waking period. Following the third night on this schedule, subjects underwent another 24-hour measurement period. During both measurement periods, blood samples were collected and PBMCs were isolated. mRNA was extracted, labelled, and hybridized to microarrays.
2019-02-14 | GSE122725 | GEO
Project description:Detecting Circadian Rhythmicity By Single Cell Multiomics
| PRJNA1218624 | ENA
Project description:Membrane type I-matrix metalloproteinase (MT1-MMP/Mmp14) is an unusual MMP because it is essential for survival in mice with multiple organ systems being affected for reasons that are unclear. Here, we show that the protein (MT1-MMP) and gene (Mmp14) are under strict circadian clock control and conditional knockout in fibroblasts leads to ~16% of the proteome losing or inverting circadian rhythmicity. The result is loss of the actin cytoskeleton and cell-matrix adhesions and major imbalance of the matrisome. Lack of collagen-I monomer turnover results in excess fibril formation in the absence of Mmp14. In the absence of Mmp14, paired-like homeodomain transcription factor 2 (Pitx2) is upregulated and remains in the nucleus where it drives Plod2 expression. The overall result is accumulation of collagen fibrils and elevated pyridinoline crosslinking that renders collagen fibrils insoluble. In conclusion, Mmp14 is a master regulator of circadian rhythms affecting the actin cytoskeleton and cell microenvironment.
2023-10-31 | PXD031692 | Pride
Project description:Circadian rhythmicity of gene expression is a conserved feature of cell physiology. This involves fine tuning between transcriptional and post-transcriptional molecular mechanisms, strongly dependent on the metabolic state of the cell, which guarantees adaptive plasticity of tissue-specific genetic programs. Dynamics of epigenome structure and epigenetic regulators support this plasticity. However, the intermingle between epigenome and RNA Pol II rhythmicity remains to be investigated. Here we identify the Polycomb group (PcG) protein EZH1 as a gateway bridging function regulating periodic alternation between chromatin mediated silencing and active transcription in post-mitotic skeletal muscle cells. We show that PRC2-EZH1 core components are under direct regulation of BMAL1, and show an oscillatory behavior and a regulated periodic assembly of PRC2-EZH1 complex. Instead at alternate Zeitgeber points, EZH1 becomes essential for circadian gene expression, through stabilization of RNA Pol II preinitiation complex controlling nascent transcription process. Collectively, our data show that EZH1 depending on the stoichiometry of its partners guarantees both negative and positive modulation of RNA Pol II activity, resulting in oscillatory transcription.
2024-10-11 | PXD035453 | Pride
Project description:Background. Inter- and intra-individual fluctuations in pain intensity pose a major challenge to treatment efficacy, with a majority perceiving their pain relief as inadequate. Recent preclinical studies have identified circadian rhythmicity as a potential contributor to these fluctuations and therapeutic target. Methods. We therefore sought to determine the impact of these rhythms in people with chronic low back pain (CLBP) through a detailed characterization, including questionnaires to evaluate biopsychosocial characteristics, ecological momentary assessment (7-day e-diaries at 8:00/14:00/20:00) to assess pain fluctuations, and intra-day blood transcriptomics (8:00/20:00) to identify genes/pathways of interest. Results. While most individuals displayed constant or variable/mixed pain phenotypes, a distinct subset had daily fluctuations of increasing pain scores (>30% change in intensity over 12-hours in ≥4/7 days). This population had no opioid users, better biopsychosocial profiles, and differentially expressed transcripts relative to other pain phenotypes. The circadian-governed neutrophil degranulation pathway was particularly enriched among arhythmic individuals; the link between neutrophil degranulation and opioid use was further confirmed in a separate CLBP cohort. Conclusion. Our findings identify pain rhythmicity and the circadian expression of neutrophil degranulation pathways as indicators of CLBP outcomes, which may help provide a personalized approach to phenotyping biopsychosocial characteristics and medication use. This highlights the need to better understand the impact of circadian rhythmicity across chronic pain conditions.
2025-07-16 | GSE295758 | GEO
Project description:Circadian rhythmicity of gene expression is a conserved feature of cell physiology. This involves the fine tuning between transcriptional and post-transcriptional molecular mechanisms, strongly dependent on the metabolic state of the cell that guarantees intrinsic plasticity of tissue specific genetic programs. To support the plastic properties a key role is played by the dynamics of epigenome structure and its regulators. Here we investigate the role of the Polycomb cell memory complex PRC2-EZH1 in regulating transcriptional rhythmicity in post-mitotic skeletal muscle cells. We show that PRC2-EZH1 core components are under direct regulation of BMAL1, show an oscillatory behavior and control both silencing and activation of target genes. Fully assembled PRC2-EZH1 complex negatively regulates cyclic expression of direct targets through modulation of cyclic H3K27me3 status. Conversely, we show that EZH1 regulates constitutive circadian genes expression, through stabilization of RNA Pol II machinery and maintenance of transcription process fidelity. Collectively, these findings unveil the dual and multi role of PcG in circadian gene regulation in adult skeletal muscle cells, and the plastic nature of PcG cell memory system in somatic cells.
2025-01-03 | GSE198409 | GEO
Project description:Humans have a circadian rhythm for which the period varies among individuals. In the present study, we investigated the amount of natural phase delay of circadian rhythms after spending a day under dim light (Day 1 to Day 2) and the amount of phase advance due to light exposure (8000 lx, 4100 K) the following morning (Day 2 to Day 3). The relationships of the phase shifts with the circadian phase, chronotype and sleep habits were also investigated. Dim light melatonin onset (DLMO) was investigated as a circadian phase marker on each day. In the 27 individuals used for the analysis, DLMO was delayed significantly (-0.24 ± 0.33 h, p < 0.01) from Day 1 to Day 2 and DLMO was advanced significantly (0.18 ± 0.36 h, p < 0.05) from Day 2 to Day 3. There was a significant correlation between phase shifts, with subjects who had a greater phase delay in the dim environment having a greater phase advance by light exposure (r = -0.43, p < 0.05). However, no significant correlations with circadian phase, chronotype or sleep habits were found. These phase shifts may reflect the stability of the phase, but do not account for an individual's chronotype-related indicators.
| S-EPMC10594521 | biostudies-literature
Project description:This study employs advanced single cell multiomics to map the transcriptomic and epigenomic landscapes of liver peripheral clocks. By integrating these data, the research identifies core circadian genes, such as Bmal1, Clock, Per1, and Per2, exhibiting cyclic patterns across liver cell populations. Additionally, the study uncovers cell-type- and cell-state-specific cyclic genes, providing new insights into the circadian regulation tailored to the liver’s diverse metabolic functions.
2026-02-04 | GSE288579 | GEO
Project description:Group 3 innate lymphoid cells (ILC3) are major regulators of inflammation, infection, microbiota composition and metabolism. ILC3 and neuronal cells were shown to interact at discrete mucosal locations to steer mucosal defence. Nevertheless, whether neuroimmune circuits operate at an organismal level, integrating extrinsic environmental signals to orchestrate ILC3 responses remains elusive. Here we show that light-entrained and brain-tuned circadian circuits regulate enteric ILC3, intestinal homeostasis and the host lipid metabolism. We found that enteric ILC3 display circadian expression of clock genes and ILC3-related transcription factors. ILC3-autonomous ablation of the circadian regulator Arntl led to disrupted gut ILC3 homeostasis, impaired epithelial reactivity, deregulated microbiome, increased susceptibility to bowel infection and disrupted lipid metabolism. Loss of ILC3-intrinsic Arntl shaped the gut postcode receptors of ILC3. Strikingly, light-dark cycles, feeding rhythms and microbial cues differentially regulated ILC3 clocks, with light signals as major entraining cues of ILC3. Accordingly, surgical- and genetically-induced deregulation of brain rhythmicity led to disrupted circadian ILC3 oscillations, deregulated microbiome and altered lipid metabolism. Our work reveals a circadian circuitry that translates environmental light cues into enteric ILC3, shaping intestinal health and organismal homeostasis.
2019-08-02 | GSE135235 | GEO
Project description:Disruption of the circadian clock as well as reduced NAD+ levels are both hallmarks of aging. While circadian rhythms and NAD+ metabolism have been linked in heart disease, their relationship during cardiac aging is less clear. Here, we show that aging leads to disruption of diurnal gene expression in the heart. Long-term supplementation with the NAD+ precursor nicotinamide riboside (NR) boosts NAD+ levels, reprograms the diurnal transcriptome, and reverses naturally occurring cardiac enlargement in aged female mice. In addition, drastic reduction of NAD+ levels in CMs impairs PER2::luc oscillations, which is rescued by NR supplementation. Finally, we demonstrate that changes to the cardiac transcriptome due to NR treatment partially depend on the activity of SIRT1. These findings reveal an essential role for NAD+ in regulation of the cardiac circadian clock upon aging, which opens up new avenues to counteract age-related cardiac disorders.
2026-02-13 | GSE240483 | GEO