Defining the Independence of the Liver Circadian Clock
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA548674 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9290770.fastq.gz | Fastqsanger.gz | |||
| SRR9290780.fastq.gz | Fastqsanger.gz | |||
| SRR9290771.fastq.gz | Fastqsanger.gz | |||
| SRR9290781.fastq.gz | Fastqsanger.gz | |||
| SRR9290772.fastq.gz | Fastqsanger.gz |
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Project description:Mammals rely on a network of circadian clocks to control daily systemic metabolism and physiology. The central pacemaker in the suprachiasmatic nucleus (SCN) is considered hierarchically dominant over peripheral clocks, whose degree of independence, or tissue-level autonomy, has never been ascertained in vivo. Using arrhythmic Bmal1-null mice, we generated animals with reconstituted circadian expression of BMAL1 exclusively in the liver (Liver-RE). High-throughput transcriptomics and metabolomics show that the liver has independent circadian functions specific for metabolic processes such as the NAD+ salvage pathway and glycogen turnover. However, although BMAL1 occupies chromatin at most genomic targets in Liver-RE mice, circadian expression is restricted to ∼10% of normally rhythmic transcripts. Finally, rhythmic clock gene expression is lost in Liver-RE mice under constant darkness. Hence, full circadian function in the liver depends on signals emanating from other clocks, and light contributes to tissue-autonomous clock function.
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Project description:As a circadian organ, liver executes diverse functions in different phase of the circadian clock. This process is believed to be driven by a transcription program. Here, we present a TF DNA-binding activity centered multi-dimensional proteomics landscape, including DNA-binding activity of TFs, the phosphorylation pattern, ubiquitylation pattern, the nuclear sub-proteome, the whole proteome as well as the transcriptome, to portrait the hierarchical circadian clock network of mouse liver. The TF DNA-binding activity indicates diurnal oscillation in four major pathways, immune response, glucose metabolism, fatty acid metabolism, and the cell cycle. We also isolated the mouse liver Kupffer cells and measured their proteomes in the circadian clock to reveal cell type resolved circadian clock. These are the most comprehensive datasets for circadian clock in the mouse liver and provided the richest data resource for the understanding of mouse liver physiology around the circadian clock.
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Project description:Mammals rely on a network of circadian clocks to control daily systemic metabolism and physiology. The central pacemaker in the suprachiasmatic nucleus (SCN) is considered hierarchically dominant over peripheral clocks, whose degree of independence, or tissue-level autonomy, has never been ascertained in vivo. Using arrhythmic Bmal1-null mice, we generated animals with reconstituted circadian expression of BMAL1 exclusively in the liver (Liver-RE). High-throughput transcriptomics and metabolomics show that the liver has independent circadian functions specific for metabolic processes such as the NAD+ salvage pathway and glycogen turnover. However, although BMAL1 occupies chromatin at most genomic targets in Liver-RE mice, circadian expression is restricted to ∼10% of normally rhythmic transcripts. Finally, rhythmic clock gene expression is lost in Liver-RE mice under constant darkness. Hence, full circadian function in the liver depends on signals emanating from other clocks, and light contributes to tissue-autonomous clock function.
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Project description:The mammalian circadian clock system is made up of individual cell and tissue clocks that function as a coherent network, however it remains unclear which rhythmic functions of the liver clock are autonomous or rely on clocks in other tissues. Here, using mice which only have a functioning liver clock, we investigate the autonomous vs non-autonomous reatures of the liver clock and diurnal rhythmicity in the liver
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Project description:As a circadian organ, liver executes diverse functions in different phase of the circadian clock. This process is believed to be driven by a transcription program. Here, we present a TF DNA-binding activity centered multi-dimensional proteomics landscape, including DNA-binding activity of TFs, the phosphorylation pattern, ubiquitylation pattern, the nuclear sub-proteome, the whole proteome as well as the transcriptome, to portrait the hierarchical circadian clock network of mouse liver. The TF DNA-binding activity indicates diurnal oscillation in four major pathways, immune response, glucose metabolism, fatty acid metabolism, and the cell cycle. We also isolated the mouse liver Kupffer cells and measured their proteomes in the circadian clock to reveal cell type resolved circadian clock. These are the most comprehensive datasets for circadian clock in the mouse liver and provided the richest data resource for the understanding of mouse liver physiology around the circadian clock.
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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.
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