Impact of circadian time, feeding-fasting rhythm and the autonomous clock on the transcriptome
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ABSTRACT:
PROVIDER: PRJNA665741 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12714600_1.fastq.gz | Fastqsanger.gz | |||
| SRR12714600_2.fastq.gz | Fastqsanger.gz | |||
| SRR12714601_1.fastq.gz | Fastqsanger.gz | |||
| SRR12714601_2.fastq.gz | Fastqsanger.gz | |||
| SRR12714602_1.fastq.gz | Fastqsanger.gz |
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Project description:Using an "omics"-based approach, we investigated the interaction between the autonomous liver clock and feeding-fasting rhythm. Transcriptomic analysis and subsequent quantification of exonic and intronic reads revealed that transcriptional mechanisms mediate, at least in part, the integration of feeding signals by the liver clock to drive mRNA oscillations. Therefore, we performed ATAC-seq to probe the state of chromatin accessibility genome-wide. While most open chromatin regions are unchanged across genotype, time and feeding status, transcription factor (TFs) footprints showed altered activity of certain TFs in Liver-RE AL vs NF. For example, CEBPB activity is altered in Liver-RE AL and restored in NF, an observation accompanied by restored CEBPB and BMAL1 common target gene oscillations. Finally, metabolomics analysis illustrated the partial rescue of hepatic metabolism in Liver-RE NF compared to AL (extensive carbohydrate pathway oscillations), and made clear that extra-hepatic clocks contribute significantly to metabolic oscillations in the liver, particularly for pathways involving lipids. Please see the associated reference for full results.
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Project description:Using an "omics"-based approach, we investigated the interaction between the autonomous liver clock and feeding-fasting rhythm. Transcriptomic analysis and subsequent quantification of exonic and intronic reads revealed that transcriptional mechanisms mediate, at least in part, the integration of feeding signals by the liver clock to drive mRNA oscillations. Therefore, we performed ATAC-seq to probe the state of chromatin accessibility genome-wide. While most open chromatin regions are unchanged across genotype, time and feeding status, transcription factor (TFs) footprints showed altered activity of certain TFs in Liver-RE AL vs NF. For example, CEBPB activity is altered in Liver-RE AL and restored in NF, an observation accompanied by restored CEBPB and BMAL1 common target gene oscillations. Finally, metabolomics analysis illustrated the partial rescue of hepatic metabolism in Liver-RE NF compared to AL (extensive carbohydrate pathway oscillations), and made clear that extra-hepatic clocks contribute significantly to metabolic oscillations in the liver, particularly for pathways involving lipids. Please see the associated reference for full results.
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Project description:Impact of circadian time, feeding-fasting rhythm and the autonomous clock on chromatin accessibility
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Project description:Increased susceptibility of circadian clock mutant mice to metabolic diseases has led to the understanding that a molecular circadian clock is necessary for metabolic homeostasis. Circadian clock produces a daily rhythm in activity-rest and an associated rhythm in feeding-fasting. Feeding-fasting driven programs and cell autonomous circadian oscillator act synergistically in the liver to orchestrate daily rhythm in metabolism. However, an imposed feeding-fasting rhythm, as in time-restricted feeding, can drive some rhythm in liver gene expression in clock mutant mice. We tested if TRF alone, in the absence of a circadian clock in the liver or in the whole animal can prevent obesity and metabolic syndrome. Mice lacking the clock component Bmal1 in the liver, Rev-erb alpha/beta in the liver or cry1-/-;cry2-/- (CDKO) mice rapidly gain weight and show genotype specific increased susceptibility to dyslipidemia, hypercholesterolemia and glucose intolerance under ad lib fed condition. However, when the mice were fed the same diet under time-restricted feeding regimen that imposed 10 h feeding during the night, they were protected from weight gain and other metabolic diseases. Transcriptome and metabolome analyses of the liver from there mutant mice showed TRF reduces de novo lipogenesis, increased beta-oxidation independent of a circadian clock. TRF also enhanced cellular defense to metabolic stress. These results suggest a major function of the circadian clock in metabolic homeostasis is to sustain a daily rhythm in feeding and fasting. The feeding-fasting cycle orchestrates a balance between nutrient stress and cellular response to maintain homeostasis.
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