Ontology highlight
ABSTRACT:
PROVIDER: PRJNA632844 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11789818_1.fastq.gz | Fastqsanger.gz | |||
| SRR11789818_2.fastq.gz | Fastqsanger.gz | |||
| SRR11789819_1.fastq.gz | Fastqsanger.gz | |||
| SRR11789819_2.fastq.gz | Fastqsanger.gz | |||
| SRR11789820_1.fastq.gz | Fastqsanger.gz |
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Project description:Meal timing is essential in synchronization of circadian rhythms in different organ systems through clock-dependent and -independent mechanisms. The liver is a critical metabolic organ whose circadian clock and transcriptome can be readily reset by meal timing. However, it remains largely unexplored how circadian rhythms in the liver are organized in time-restricted feeding that intervenes meal timing. Here, we applied data-independent acquisition proteomics to characterize circadian features associated with day/sleep- (DRF) and night/wake (NRF)-time restricted feeding in nocturnal female mice. The transcriptomics and metabolomics datasets are public (see www.circametdb.org.cn).
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Project description:Meal timing is essential in synchronization of circadian rhythms in different organ systems through clock-dependent and -independent mechanisms. The liver is a critical metabolic organ whose circadian clock and transcriptome can be readily reset by meal timing. However, it remains largely unexplored how circadian rhythms in the liver are organized in time-restricted feeding that intervenes meal timing. Here, we applied affinity-purification based shotgun proteomics for ubiquitylation to characterize circadian features associated with day/sleep- (DRF) and night/wake (NRF)-time restricted feeding in nocturnal female mice. The transcriptomics and metabolomics datasets are public (see www.circametdb.org.cn).
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Project description:Meal timing is essential in synchronization of circadian rhythms in different organ systems through clock-dependent and -independent mechanisms. The liver is a critical metabolic organ whose circadian clock and transcriptome can be readily reset by meal timing. However, it remains largely unexplored how circadian rhythms in the liver are organized in time-restricted feeding that intervenes meal timing. Here, we applied affinity-purification based shotgun proteomics for N-glycosylation to characterize circadian features associated with day/sleep- (DRF) and night/wake (NRF)-time restricted feeding in nocturnal female mice. The transcriptomics and metabolomics datasets are public (see www.circametdb.org.cn).
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Project description:Meal timing is essential in synchronization of circadian rhythms in different organ systems through clock-dependent and -independent mechanisms. The liver is a critical metabolic organ whose circadian clock and transcriptome can be readily reset by meal timing. However, it remains largely unexplored how circadian rhythms in the liver are organized in time-restricted feeding that intervenes meal timing. Here, we applied affinity-purification based shotgun proteomics for protein phosphorylation to characterize circadian features associated with day/sleep- (DRF) and night/wake (NRF)-time restricted feeding in nocturnal female mice. The transcriptomics and metabolomics datasets are public (see www.circametdb.org.cn).
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Project description:Meal timing is essential in synchronization of circadian rhythms in different organ systems through clock-dependent and -independent mechanisms. The liver is a critical metabolic organ whose circadian clock and transcriptome can be readily reset by meal timing. However, it remains largely unexplored how circadian rhythms in the liver are organized in time-restricted feeding that intervenes meal timing. Here, we applied affinity-purification based shotgun proteomics for succinylation to characterize circadian features associated with day/sleep- (DRF) and night/wake (NRF)-time restricted feeding in nocturnal female mice. The transcriptomics and metabolomics datasets are public (see www.circametdb.org.cn).
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Project description:The circadian clock and rhythmic food intake are both important regulators of rhythmic gene expression in the liver. It remains, however, elusive to which extent the circadian clock network and natural feeding rhythms contribute to rhythmic gene expression. To systematically address this question, we developed an algorithm to investigate differential rhythmicity between a varying number of conditions. Mouse knockout models of different parts of the circadian clock network (Bmal1, Cry1/2, and Hlf/Dbp/Tef) exposed to controlled feeding regimens (ad libitum, night restricted feeding) were generated and analyzed for their temporal hepatic transcriptome. A genetical ablation of core loop elements altered feeding patterns that were restored by night restricted feeding. Mainly genes with a high amplitude were driven by the circadian clock but natural feeding patterns equally contributed to rhythmic gene expression with lower amplitude. We observed that Bmal1 and Cry1/2 KOs differed in rhythmic gene expression and identified differences in mean expression levels as a predictor for rhythmic gene expression. In Hlf/Dbp/Tef KO, mRNA levels of Hlf/Dbp/Tef target genes were decreased, albeit rhythmicity was overall preserved potentially due to the activity of the D-Box binding repressor NFIL3. Genes that lost rhythmicity in Hlf/Dbp/Tef KOs were identified to be no direct targets of PARbZip factors and presumably lost rhythmicity due to indirect effects. Collectively, our findings provide unprecedent insights into the diurnal transcriptome in mouse liver and defines the contribution of subloops of the circadian clock network and natural feeding cycles. The developed algorithm and a webapp to browse the outcomes of the study are publicly available to serve as a resource for the scientific community.
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Project description:The circadian clock and rhythmic food intake are both important regulators of rhythmic gene expression in the liver. It remains, however, elusive to which extent the circadian clock network and natural feeding rhythms contribute to rhythmic gene expression. To systematically address this question, we developed an algorithm to investigate differential rhythmicity between a varying number of conditions. Mouse knockout models of different parts of the circadian clock network (Bmal1, Cry1/2, and Hlf/Dbp/Tef) exposed to controlled feeding regimens (ad libitum, night restricted feeding) were generated and analyzed for their temporal hepatic transcriptome. A genetical ablation of core loop elements altered feeding patterns that were restored by night restricted feeding. Mainly genes with a high amplitude were driven by the circadian clock but natural feeding patterns equally contributed to rhythmic gene expression with lower amplitude. We observed that Bmal1 and Cry1/2 KOs differed in rhythmic gene expression and identified differences in mean expression levels as a predictor for rhythmic gene expression. In Hlf/Dbp/Tef KO, mRNA levels of Hlf/Dbp/Tef target genes were decreased, albeit rhythmicity was overall preserved potentially due to the activity of the D-Box binding repressor NFIL3. Genes that lost rhythmicity in Hlf/Dbp/Tef KOs were identified to be no direct targets of PARbZip factors and presumably lost rhythmicity due to indirect effects. Collectively, our findings provide unprecedent insights into the diurnal transcriptome in mouse liver and defines the contribution of subloops of the circadian clock network and natural feeding cycles. The developed algorithm and a webapp to browse the outcomes of the study are publicly available to serve as a resource for the scientific community.
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