E-GEOD-59460
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA255376PRJNA255427
PROVIDER: E-GEOD-59460 | ExpressionAtlas | 2015-01-28
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-59460-analysis-methods.tsv | Tabular | |||
| E-GEOD-59460-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-59460-configuration.xml | Xml | |||
| E-GEOD-59460-percentile-ranks.tsv | Tabular | |||
| E-GEOD-59460.condensed-sdrf.tsv | Tabular |
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Project description:Mammalian transcriptomes display complex circadian rhythms with multiple phases of gene expression that cannot be accounted for by current models of the molecular clock. We have determined the underlying mechanisms by measuring nascent RNA transcription around the clock in mouse liver. Unbiased examination of eRNAs that cluster in specific circadian phases identified functional enhancers driven by distinct transcription factors (TFs). We further identify on a global scale the components of the TF cistromes that function to orchestrate circadian gene expression. Integrated genomic analyses also revealed novel mechanisms by which a single circadian factor controls opposing transcriptional phases. These findings shed new light on the diversity and specificity of TF function in the generation of multiple phases of circadian gene transcription in a mammalian organ. The goal of this experiment was to determine direct targets of Rev-erb{alpha} in mouse liver. All samples were collected at ZT10, when Rev-erb{alpha} protein levels and genomic binding are maximal. All mice were housed and harvested together (n=5 per genotype). All mice were male, 10-12 week old on C57Bl/6 background. RNA was extracted, processed, and hybridized from each mouse liver individually (each sample represents a single mouse).
2015-01-06 | E-GEOD-59460 | biostudies-arrayexpress
Project description:Mammalian transcriptomes display complex circadian rhythms with multiple phases of gene expression that cannot be accounted for by current models of the molecular clock. We have determined the underlying mechanisms by measuring nascent RNA transcription around the clock in mouse liver. Unbiased examination of eRNAs that cluster in specific circadian phases identified functional enhancers driven by distinct transcription factors (TFs). We further identify on a global scale the components of the TF cistromes that function to orchestrate circadian gene expression. Integrated genomic analyses also revealed novel mechanisms by which a single circadian factor controls opposing transcriptional phases. These findings shed new light on the diversity and specificity of TF function in the generation of multiple phases of circadian gene transcription in a mammalian organ. The goal of this experiment was to determine direct targets of Rev-erb{alpha} in mouse liver. All samples were collected at ZT10, when Rev-erb{alpha} protein levels and genomic binding are maximal.
2015-01-06 | GSE59460 | GEO
Project description:Using chromatin immuno-precipitation (ChIP) combined with deep sequencing (ChIP-seq) we obtained a time resolved and genome-wide map of BMAL1 binding in mouse liver, which allowed to identify over two thousand binding sites with peak binding narrowly centered around Zeitgeber time (ZT) 6. Annotation of BMAL1 targets confirms carbohydrate and lipid metabolism as the major output of the circadian clock in mouse liver. Moreover, transcription regulators are largely overrepresented, several of which also exhibit circadian activity. Genes of the core circadian oscillator stand out as strongly bound, often at promoter and distal sites. Genomic sequence analysis of the sites identified E- boxes and tandem E1-E2 consensus elements. Electromobility shift assays (EMSA) showed that E1-E2 sites are bound by a dimer of BMAL1/CLOCK heterodimers with a spacing-dependent cooperative interaction that was further validated in transactivation assays. BMAL1 target genes showed cyclic mRNA expression profiles with a phase distribution centered at ZT10. Importantly, sites with E1-E2 elements showed tighter phases both in binding and mRNA accumulation. Finally, comparing the temporal accumulation of precursor mRNA and mature mRNA helped distinguish direct BMAL1 targets from targets with more complex regulation, and showed how transcriptional and post-transcriptional regulation contribute differentially to circadian expression phase. Together, our analysis of a dynamic protein-DNA interactome uncovered how genes of the core circadian oscillator are wired together and drive phase-specific circadian output programs in a complex tissue. ChIP-Seq of BMAL1 in mouse liver during one circadian cycle at 4 hour time resolution presented in this Series (GSE26602). mRNA profiling data used in this study are already published (Kornmann et al, PLoS Biol 2007) and have been deposited on ArrayExpress repository (accession number: E-MEXP-842).
2011-02-23 | E-GEOD-26602 | biostudies-arrayexpress
Project description:Obesity and liver diseases are associated with the disruption of the circadian clock that orchestrates mammalian physiology to optimize nutrient metabolism and storage. We show here that the activity of the circadian clock regulator BMAL1 is perturbed during liver fibrosis in humans. To understand the impact of BMAL1 perturbation in obesity and liver diseases, we assessed the impact of a high fat diet or leptin deficiency on Bmal1 knockout mice. While Bmal1 knockout mice were prone to obesity, they were protected against insulin resistance, hepatic steatosis, inflammation, and fibrosis. In addition to direct transcriptional regulation of metabolic programs by BMAL1, we show that adaptation disruption of the growth hormone and sex hormone pathways plays a critical role in this protection. Similar endocrine perturbations correlate with the development of liver fibrosis in humans, but were absent in hepatocyte specific Bmal1 knockout mice. This suggestsing that systemic endocrine perturbation associated with circadian disruptionthe disruption of BMAL1 activity is critical for the pathogenesis of metabolic and liver diseases.
2022-01-26 | GSE150102 | GEO
Project description:We previously reported that neutrophils infiltrate most tissues in a circadian fashion, as they clear out from the circulation (Casanova‑Acebes et al., 2018). In our current study we hypothesized that neutrophils are relevant contributors to the matrix of barrier tissues and that then their elimination should leave a temporal footprint in the circadian pattern of expression of matrix-associated genes. To answer this question, we generated a circadian transcriptional dataset from the bone marrow, lung, liver, intestine and skin in wild type and neutrophil-depleted animals. The anlysis of the circadian patern of matrix related genes obtained from this datasets indicates that their temporal expression patterns in the analysed tissues is disrupted following neutrophil depletion. This results directly implicate neutrophils in the circadian biology of the matrix organization in various tissues.
2025-01-09 | GSE198770 | GEO
Project description:Circadian rhythms are integral to maintaining metabolic health by temporally coordinating metabolic functions across tissues. However, the mechanisms underlying circadian cross-tissue coordination remain poorly understood. In this study, we uncover a central role for the liver clock in regulating circadian rhythms in white adipose tissue (WAT). Using a liver-specific Bmal1 knockout mouse model, we show that hepatic circadian control is crucial for lipid metabolism in WAT. In addition, by utilizing a model where functional clocks are restricted to the liver, we demonstrate that the liver clock alone drives circadian gene expression in WAT, including Cebpa, a key regulator of adipogenesis. Mechanistically, we show that circadian liver-to-WAT communication is mediated through secreted proteins, including the adaptor protein 14-3-3η (Ywhah). The clinical relevance of these findings is supported by human cohort data, which correlate liver YWHAH expression with lipid metabolic pathways in WAT and cardiometabolic risk factors. These findings provide a mechanistic framework for how the liver clock coordinates WAT physiology and highlights its central role in cardiometabolic health, offering potential insights for targeted circadian-based therapies for metabolic disorders.
2025-02-11 | GSE288748 | GEO
Project description:Circadian rhythms are integral to maintaining metabolic health by temporally coordinating metabolic functions across tissues. However, the mechanisms underlying circadian cross-tissue coordination remain poorly understood. In this study, we uncover a central role for the liver clock in regulating circadian rhythms in white adipose tissue (WAT). Using a liver-specific Bmal1 knockout mouse model, we show that hepatic circadian control is crucial for lipid metabolism in WAT. In addition, by utilizing a model where functional clocks are restricted to the liver, we demonstrate that the liver clock alone drives circadian gene expression in WAT, including Cebpa, a key regulator of adipogenesis. Mechanistically, we show that circadian liver-to-WAT communication is mediated through secreted proteins, including the adaptor protein 14-3-3η (Ywhah). The clinical relevance of these findings is supported by human cohort data, which correlate liver YWHAH expression with lipid metabolic pathways in WAT and cardiometabolic risk factors. These findings provide a mechanistic framework for how the liver clock coordinates WAT physiology and highlights its central role in cardiometabolic health, offering potential insights for targeted circadian-based therapies for metabolic disorders.
2025-02-11 | GSE288747 | GEO
Project description:Circadian rhythms are integral to maintaining metabolic health by temporally coordinating metabolic functions across tissues. However, the mechanisms underlying circadian cross-tissue coordination remain poorly understood. In this study, we uncover a central role for the liver clock in regulating circadian rhythms in white adipose tissue (WAT). Using a liver-specific Bmal1 knockout mouse model, we show that hepatic circadian control is crucial for lipid metabolism in WAT. In addition, by utilizing a model where functional clocks are restricted to the liver, we demonstrate that the liver clock alone drives circadian gene expression in WAT, including Cebpa, a key regulator of adipogenesis. Mechanistically, we show that circadian liver-to-WAT communication is mediated through secreted proteins, including the adaptor protein 14-3-3η (Ywhah). The clinical relevance of these findings is supported by human cohort data, which correlate liver YWHAH expression with lipid metabolic pathways in WAT and cardiometabolic risk factors. These findings provide a mechanistic framework for how the liver clock coordinates WAT physiology and highlights its central role in cardiometabolic health, offering potential insights for targeted circadian-based therapies for metabolic disorders.
2025-02-11 | GSE288746 | GEO
Project description:Obesity and liver diseases are associated with the disruption of the circadian clock that orchestrates mammalian physiology to optimize nutrient metabolism and storage. We show here that the activity of the circadian clock regulator BMAL1 is perturbed during liver fibrosis in humans. To understand the impact of BMAL1 perturbation in obesity and liver diseases, we assessed the impact of a high fat diet or leptin deficiency on Bmal1 knockout mice. While Bmal1 knockout mice were prone to obesity, they were protected against insulin resistance, hepatic steatosis, inflammation, and fibrosis. In addition to direct transcriptional regulation of metabolic programs by BMAL1, we show that adaptation of the growth hormone and sex hormone pathways plays a critical role in this protection. Similar endocrine perturbations correlate with the development of liver fibrosis in humans, suggesting that endocrine perturbation associated with circadian disruption is critical for the pathogenesis of metabolic and liver diseases.
2022-01-26 | GSE190221 | GEO
Project description:The PAR-domain basic leucine zipper (PAR bZip) transcription factors DBP, TEF, and HLF accumulate in a highly circadian manner in several peripheral tissues, including liver and kidney. Mice devoid of all three of these proteins are born at expected Mendelian ratios, but are epilepsy-prone, age at an accelerated rate and die prematurely. In the hope of identifying PAR bZip target genes whose altered expression might contribute to the high morbidity and mortality of PAR bZip triple knockout mice, we compared the liver and kidney transcriptomes of these animals to those of wild-type or heterozygous mutant mice. These experiments revealed that PAR bZip proteins control the expression of many enzymes and regulators involved in detoxification and drug metabolism, such as cytochrome P450 enzymes, carboxylesterases, and constitutive androstane receptor (CAR). Indeed, PAR bZip triple knockout mice are hypersensitive to xenobiotic compounds, and the deficiency in detoxification may contribute to their early ageing.
2006-12-20 | E-MEXP-565 | biostudies-arrayexpress