Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA273743 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Circadian Rhythm of Gene Expression Patterns in Liver of Mouse
| PRJNA106349 | ENA
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.
2025-12-01 | GSE266937 | GEO
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.
2025-12-01 | GSE266936 | GEO
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.
2025-12-01 | GSE266938 | GEO
Project description:Post-transcriptional regulation of circadian rhythm by miRNA in mouse liver
| PRJNA255284 | ENA
Project description:Circadian rhythm disruption is associated with skeletal muscle dysfunction within the blind Mexican Cavefish
2023-01-13 | MSV000091062 | MassIVE
Project description:We examined the biological difference between H1299 cells with the treatments targeting circadian rhythm in order to better understand circadian rhythm disruption as a feature of cancer. To this end, we knocked down CLOCK using siRNA (siCLOCK) or melatonin pre-treatment and assessed the gene expression pattern by RNA-Seq.
2022-02-19 | GSE196848 | GEO
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.
2018-08-30 | GSE102072 | GEO
Project description:The liver circadian clock and hepatic transcriptome are highly responsive to metabolic signals generated from feeding-fasting rhythm. Previous studies have identified a number of nutrient-sensitive signaling pathways that could interpret metabolic input to regulate rhythmic hepatic biology. Here, we investigated the role of O-GlcNAcylation, a nutrient-sensitive post-translational modification (PTM) in mediating metabolic regulation of rhythmic biology in the liver. We observed daily oscillation of global nuclear protein O-GlcNAcylation in the liver of mice subjected to night-restricted feeding (NRF). Among 449 O-GlcNAcylated proteins we identified, 64 proteins are rhythmically O-GlcNAcylated over a 24-hour day-night cycle. Proteins involved in gene expression were enriched among rhythmically O-GlcNAcylated nuclear proteins, suggesting rhythmic O-GlcNAcylation may directly shape the daily rhythmicity of the hepatic transcriptome. We also identified xxx O-GlcNAcylation sites, demonstrating day-night differences of site-specific O-GlcNAcylation. Furthermore, we showed that rhythmic O-GlcNAcylation can also indirectly modulate the hepatic transcriptome by interacting with phosphorylation. Specifically, several proteins harboring O-GlcNAcylation-phosphorylation interplay motif exhibit rhythmic O-GlcNAcylation and phosphorylation. We show that O-GlcNAcylation occur at a phospho-degron of a key circadian transcriptional activator, circadian locomotor output cycles kaput (CLOCK), thus regulating its stability and transcriptional output. Finally, we report that day-restricted feeding (DRF) in the nocturnal mouse dampens O-GlcNAcylation rhythm. This suggests the dysregulation of daily nuclear protein O-GlcNAcylation rhythm could partially contribute to the disruption in liver transcriptomic rhythm previously observed in DRF condition, despite not the primary driver. In summary, our results provide new mechanistic insights into metabolic regulation of daily hepatic transcriptomic rhythm via interplay between O-GlcNAcylation and phosphorylation and shed light on the deleterious effects of improper mealtimes.
2025-05-13 | MSV000097856 | MassIVE