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:Sex differences in liver gene expression are dictated by sex-differences in circulating growth hormone (GH) profiles. Presently, the pituitary hormone dependence of mouse liver gene expression was investigated on a global scale to discover sex-specific early GH response genes that might contribute to sex-specific regulation of downstream GH targets and to ascertain whether intrinsic sex-differences characterize hepatic responses to plasma GH stimulation. RNA expression analysis using 41,000-feature microarrays revealed two distinct classes of sex-specific mouse liver genes: genes subject to positive regulation (class-I) and genes subject to negative regulation by pituitary hormones (class-II). Genes activated or repressed in hypophysectomized (Hypox) mouse liver within 30-90min of GH pulse treatment at a physiological dose were identified as direct targets of GH action (early response genes). Intrinsic sex-differences in the GH responsiveness of a subset of these early response genes were observed. Notably, 45 male-specific genes, including five encoding transcriptional regulators that may mediate downstream sex-specific transcriptional responses, were rapidly induced by GH (within 30min) in Hypox male but not Hypox female mouse liver. The early GH response genes were enriched in 29 male-specific targets of the transcription factor Mef2, whose activation in hepatic stellate cells is associated with liver fibrosis leading to hepatocellular carcinoma, a male-predominant disease. Thus, the rapid activation by GH pulses of certain sex-specific genes is modulated by intrinsic sex-specific factors, which may be associated with prior hormone exposure (epigenetic mechanisms) or genetic factors that are pituitary-independent, and could contribute to sex-differences in predisposition to liver cancer or other hepatic pathophysiologies.
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