Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA258229 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11684143.fastq.gz | Fastqsanger.gz | |||
| SRR11691981.fastq.gz | Fastqsanger.gz | |||
| SRR1551960_1.fastq.gz | Fastqsanger.gz | |||
| SRR1551960_2.fastq.gz | Fastqsanger.gz | |||
| SRR1551970_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 60 |
Similar Datasets
Project description:Regulatory logic of the coupled diurnal and feeding cycles in the mouse liver
| PRJNA258563 | ENA
Project description:Regulatory logic of the coupled diurnal and feeding cycles in the mouse liver [array]
| PRJNA258564 | ENA
Project description:Physiology is regulated by interconnected cell and tissue circadian clocks. Disruption of the rhythms generated by this interconnectedness is associated with metabolic disease. Here we tested the interactions between clocks in two critical components of organismal metabolism – liver and skeletal muscle – by rescuing clock function either in each organ separately, or in both organs simultaneously, in otherwise clock-less mice. Experiments revealed that individual clocks are partially sufficient for tissue glucose metabolism, yet the connections between both tissue clocks coupled with daily feeding rhythms maximizes systemic glucose tolerance. This synergy relies in part on local transcriptional control of the glucose machinery, feeding-responsive signals such as insulin, and metabolic cycles that connect the muscle and liver. We posit that spatiotemporal mechanisms of muscle and liver play an essential role in the maintenance of systemic glucose homeostasis, and that disrupting this diurnal coordination can contribute to the metabolic disease.
2023-05-29 | GSE228389 | GEO
Project description:Hepatic daily rhythms are coordinated by feeding and the molecular circadian clock, ensuring metabolic homeostasis. Disrupted feeding schedules promote circadian misalignment and metabolic disease but the underlying mechanisms remain unknown. Post-translational modifications have emerged as key regulators of circadian metabolic outputs. In this framework, mitochondria constitute a central hub, integrating metabolic rhythms, feeding cycles and the circadian clock. Here, we show that the mitochondrial enzyme Acyl-CoA-synthetase-family-member-3 (ACSF3) oscillates in phase with different feeding schedules to drive rhythmic lysine-malonylation and coordinate daily hepatic metabolism. Hepatic ACSF3 knockdown affected lysine-malonylation rhythms, decreased fasting glycemia, insulin sensitivity and AKT phosphorylation. It also shifted lipid oxidation from mitochondria to peroxisomes, enhanced de novo lipogenesis and triglyceride synthesis, while increasing diurnal autophagy. Integrated multi-omics profiling uncovered specific lysine-malonylation targets in glycolysis, the TCA cycle, fatty-acid oxidation and autophagy. Our findings establish ACSF3 as a critical link between feeding time, protein malonylation, and diurnal liver metabolism.
2026-07-07 | PXD066863 | Pride
Project description:Hepatic daily rhythms are coordinated by feeding and the molecular circadian clock, ensuring metabolic homeostasis. Disrupted feeding schedules promote circadian misalignment and metabolic disease but the underlying mechanisms remain unknown. Post-translational modifications have emerged as key regulators of circadian metabolic outputs. In this framework, mitochondria constitute a central hub, integrating metabolic rhythms, feeding cycles and the circadian clock. Here, we show that the mitochondrial enzyme Acyl-CoA-synthetase-family-member-3 (ACSF3) oscillates in phase with different feeding schedules to drive rhythmic lysine-malonylation and coordinate daily hepatic metabolism. Hepatic ACSF3 knockdown affected lysine-malonylation rhythms, decreased fasting glycemia, insulin sensitivity and AKT phosphorylation. It also shifted lipid oxidation from mitochondria to peroxisomes, enhanced de novo lipogenesis and triglyceride synthesis, while increasing diurnal autophagy. Integrated multi-omics profiling uncovered specific lysine-malonylation targets in glycolysis, the TCA cycle, fatty-acid oxidation and autophagy. Our findings establish ACSF3 as a critical link between feeding time, protein malonylation, and diurnal liver metabolism.
2026-07-06 | PXD066866 | Pride
Project description:Liver circadian clock and daily rhythmic transcriptome are highly responsive to metabolic cues generated from daily feeding activity. The mechanisms that mediate metabolic inputs to the whole rhythmic transcriptome are still under investigation. Here, we explored the role of O-GlcNAcylation, a nutrient-sensitive post-translational modification (PTM) that integrates circadian and metabolic signals, in the diurnal regulation of nuclear proteins. We found daily oscillation of overall nuclear protein O-GlcNAcylation in the liver of mice subjected to natural night time-restricted feeding (NRF). O-GlcNAcomic analysis revealed that 11.54% of 719 O-GlcNAcylated proteins are rhythmically O-GlcNAcylated. Proteins involved in gene expression were enriched, suggesting rhythmic O-GlcNAcylation may directly shape diurnal transcriptome. Furthermore, we showed that rhythmic O-GlcNAcylation could indirectly modulate diurnal transcriptome by interacting with phosphorylation. Specifically, several proteins harboring O-GlcNAcylation-phosphorylation interplay motif exhibit rhythmic O-GlcNAcylation and phosphorylation. For example, O-GlcNAcylation may occur at a phosphor-degron of a key circadian transcriptional activator, circadian locomotor output cycles kaput (CLOCK), regulating the stability and transcriptional output of CLOCK. Lastly, unnatural day time-restricted feeding (DRF) dampens O-GlcNAcylation rhythm, suggesting the disruption of diurnal transcriptome could be mediated by protein O-GlcNAcylation. In summary, our results provide mechanistic insights into metabolic regulation of diurnal transcriptome at PTM level and shed light on the deleterious effects of improper mealtimes.
2024-03-27 | MSV000094417 | MassIVE
Project description:Sequencing files provided here are mouse liver DNase-seq for male mouse livers collected at either a peak or trough of GH/STAT5 activity. This is part of a larger study that includes DNase-seq in mouse liver from hypophysectomized males, females, and hypox-male mice given a single dose of GH. DNase hypersensitivity site (DHS) analysis of these livers established that the naturally occurring, endogenous male rhythm of plasma GH pulse-stimulated liver STAT5 activation induces dynamic, repeated cycles of chromatin opening and closing at several thousand liver DHS and comprises a novel mechanism conferring male bias to liver chromatin accessibility.
2023-08-21 | GSE131848 | GEO
Project description:Understanding the kinetics of circadian transcriptional regulation has recently advanced thanks to genome-wide dynamic mapping of RNA Polymerase II, chromatin marks such as histone 3 modifications, and several core clock regulatory factors. To obtain deeper mechanistic insights into the determinant of phase-specific transcription, we here extend previous analyses of the CycliX Consortium by integrating new genome-wide datasets enabling systematic identification of active regulatory regions in the mouse liver. DNase I hypersensitive sites (DHS)-mapping within nuclear chromatin is a powerful method to identify active regulatory elements in the genome. Experiments were performed throughout the diurnal cycle to obtain a temporal map of active regulatory elements. In addition, we quantified H3K27ac, which mark active regulatory regions, throughout the diurnal cycle and RNA Polymerase II using chromatin immunoprecipitation data analysis. DHS were validated as likely regulatory elements by footprinting analyses and overlaps with published ChIP-seq datasets. Analysis of the regions displaying diurnal patterns revealed promoter, transcription start site (TSS)-proximal and TSS-distal elements potentially involved in the regulation of rhythmic gene transcription. Peak phases of DNase I accessibility and H3K27ac levels correlated well with RNA Polymerase II loadings, and regulatory elements oscillated with phases close to those of nearest TSS, which prompted us to use these signals to infer regulatory relationships. Comparisons with results in a Bmal1 -/- genotype (KO) revealed comparable levels of diurnal transcription oscillations likely driven by nutrient and food-entrained rhythms. Using linear modeling, we inferred activities of transcription factors around the clock in WT and KO datasets to reveal that in absence of a functional core circadian clock, FOX transcription factors and glucocorticoid receptor appear to be the main drivers of phase-specific expression. This raises the interesting question of whether light-driven circadian entrainment from the central pacemaker in the SCN acts to counter effect food-related signals.
2016-12-31 | GSE60430 | GEO
Project description:Background: Cellular iron homeostasis is regulated by iron regulatory proteins (IRP1 and IRP2) that sense iron levels (and other metabolic cues) and modulate mRNA translation or stability via interaction with iron regulatory elements (IREs). IRP2 is viewed as the primary regulator in liver, yet our previous datasets showing diurnal rhythms for certain IRE-containing mRNAs suggest a nuanced temporal control mechanism. The purpose of this study is to gain insights into the daily regulatory dynamics across IRE-bearing mRNAs, specific IRP involvement, and underlying systemic and cellular rhythmicity cues in mouse liver. Results: We uncover high-amplitude diurnal oscillations in the regulation of key IRE containing transcripts in liver, compatible with maximal IRP activity at the onset of the dark phase. Although IRP2 protein levels also exhibit some diurnal variations and peak at the light-dark transition, ribosome profiling in IRP2-deficient mice reveals that maximal repression of target mRNAs at this time-point still occurs. We further find that diurnal regulation of IRE-containing mRNAs can continue in the absence of a functional circadian clock as long as feeding is rhythmic. Conclusions: Our findings suggest temporally controlled redundancy in IRP activities, with IRP2 mediating regulation of IRE-containing transcripts in the light phase and redundancy, conceivably with IRP1, at dark onset. Moreover, we highlight the significance of feeding-associated signals in driving rhythmicity. Our work highlights the dynamic nature and regulatory complexity in a metabolic pathway that had previously been considered well-understood.
2024-05-01 | GSE243134 | GEO
Project description:The goal of this study was to explore in detail how the chromatin remodeler and NuRD subunit CHD4 controls the oncogenic signature of the tumor driver and fusion protein PAX3-FOXO1 in fusion-positive rhabdomyosarcoma. To this aim, we defined the interactome of CHD4 by LC-MS, identified its location in the genome by ChIP-seq, assessed its influence on DNA accessibility by DNase I hypersensitivity assays, and determined its target genes by RNA-seq.
2020-08-11 | PXD015231 | Pride