Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA273743 | ENA |
REPOSITORIES: ENA
Similar Datasets
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Project description:The circadian rhythm in the murine liver governs the activity of numerous enhancers which in turn coordinates diurnal gene expression. This process is controlled by oscillating activities of specific transcription factors (TFs) and recruitment of co-regulators, including histone modifying enzymes and chromatin remodeling complexes. Several circadian controlled TFs interact with the SWI/SNF family of chromatin remodeling complexes to control chromatin accessibility. To unravel the significance of SWI/SNF ATPase subunits in circadian chromatin remodeling, we mapped chromatin accessibility, SWI/SNF occupancy, and gene expression throughout a day in murine liver. We found remarkable remodeling during fasting-to-fed transitions, and a third of circadian enhancers exhibited circadian SWI/SNF occupancy and accessibility. Intriguingly, genetic disruption of either of the two mutually exclusive ATPases of SWI/SNF had minor effects on chromatin accessibility in circadian enhancers, indicating redundancy. However, simultaneous disruption of both ATPases caused a collapse of the chromatin landscape, liver damage and inflammation. This disruption abolishes rhythmic expression of metabolic genes without affecting oscillation of the core circadian clock. In summary, this suggests an indispensable role of SWI/SNF-mediated chromatin remodeling of enhancers for circadian transcriptomic rhythms and basic liver function.
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Project description:The circadian rhythm in the murine liver governs the activity of numerous enhancers which in turn coordinates diurnal gene expression. This process is controlled by oscillating activities of specific transcription factors (TFs) and recruitment of co-regulators, including histone modifying enzymes and chromatin remodeling complexes. Several circadian controlled TFs interact with the SWI/SNF family of chromatin remodeling complexes to control chromatin accessibility. To unravel the significance of SWI/SNF ATPase subunits in circadian chromatin remodeling, we mapped chromatin accessibility, SWI/SNF occupancy, and gene expression throughout a day in murine liver. We found remarkable remodeling during fasting-to-fed transitions, and a third of circadian enhancers exhibited circadian SWI/SNF occupancy and accessibility. Intriguingly, genetic disruption of either of the two mutually exclusive ATPases of SWI/SNF had minor effects on chromatin accessibility in circadian enhancers, indicating redundancy. However, simultaneous disruption of both ATPases caused a collapse of the chromatin landscape, liver damage and inflammation. This disruption abolishes rhythmic expression of metabolic genes without affecting oscillation of the core circadian clock. In summary, this suggests an indispensable role of SWI/SNF-mediated chromatin remodeling of enhancers for circadian transcriptomic rhythms and basic liver function.
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Project description:The circadian rhythm in the murine liver governs the activity of numerous enhancers which in turn coordinates diurnal gene expression. This process is controlled by oscillating activities of specific transcription factors (TFs) and recruitment of co-regulators, including histone modifying enzymes and chromatin remodeling complexes. Several circadian controlled TFs interact with the SWI/SNF family of chromatin remodeling complexes to control chromatin accessibility. To unravel the significance of SWI/SNF ATPase subunits in circadian chromatin remodeling, we mapped chromatin accessibility, SWI/SNF occupancy, and gene expression throughout a day in murine liver. We found remarkable remodeling during fasting-to-fed transitions, and a third of circadian enhancers exhibited circadian SWI/SNF occupancy and accessibility. Intriguingly, genetic disruption of either of the two mutually exclusive ATPases of SWI/SNF had minor effects on chromatin accessibility in circadian enhancers, indicating redundancy. However, simultaneous disruption of both ATPases caused a collapse of the chromatin landscape, liver damage and inflammation. This disruption abolishes rhythmic expression of metabolic genes without affecting oscillation of the core circadian clock. In summary, this suggests an indispensable role of SWI/SNF-mediated chromatin remodeling of enhancers for circadian transcriptomic rhythms and basic liver function.
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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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