Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA260215 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The circadian clock in mammalian cells is cell-autonomously generated during the cellular differentiation process, but the underlying mechanisms are not understood. Here we show that perturbation of transcriptional program by constitutive expression of c-Myc and Dnmt1 ablation disrupts the differentiation-coupled emergence of the clock from mouse embryonic stem cells (ESCs). Using these model ESCs, 484 genes are identified by global gene expression analysis as factors correlated with differentiation-coupled circadian clock development. Among them, we find the misregulation of Kpna2 (Importin-α2) during the differentiation of the c-Myc over-expressed and Dnmt1-/- ESCs, in which sustained cytoplasmic accumulation of PER proteins is observed. Moreover, constitutive expression of Kpna2 during the differentiation culture of ESCs significantly impairs clock development and KPNA2 facilitates cytoplasmic localization of PER1/2. These results suggest that the programmed gene expression network regulates the differentiation-coupled circadian clock development in mammalian cells, at least in part via post-transcriptional regulation of clock proteins.
2014-11-13 | GSE61096 | GEO
Project description:The circadian clock in mammalian cells is cell-autonomously generated during the cellular differentiation process, but the underlying mechanisms are not understood. Here we show that perturbation of transcriptional program by constitutive expression of c-Myc and Dnmt1 ablation disrupts the differentiation-coupled emergence of the clock from mouse embryonic stem cells (ESCs). Using these model ESCs, 484 genes are identified by global gene expression analysis as correlating factors with differentiation-coupled circadian clock development. Among them, we find the misregulation of Kpna2 (Importin-alpha2) during the differentiation of the c-Myc over-expressed and Dnmt1-/- ESCs, in which sustaining cytoplasmic accumulation of PER proteins is observed. Moreover, constitutive expression of Kpna2 during the differentiation culture of ESCs significantly impairs clock development and KPNA2 facilitates cytoplasmic localization of PER1/2. These results suggest that the programmed gene expression network regulates the differentiation-coupled circadian clock development in mammalian cells, at least in part via post-transcriptional regulation of clock proteins.
2014-11-13 | GSE61184 | GEO
Project description:Transcriptional Program of Kpna2 (Importin-alpha2) Regulates Cellular Differentiation-Coupled Circadian Clock Development in Mammalian Cells
| PRJNA260445 | ENA
Project description:Mammalian circadian rhythms are based on coupled transcriptional-translational feedback loops driven by the transcription factors CLOCK and BMAL1. Chromatin remodeling mechanisms are essential for the proper timing and extent of circadian gene expression. We report that the S-adenosylhomocysteine (SAH) hydrolysing enzyme AHCY binds to CLOCK-BMAL1 at chromatin and drives circadian transcription by promoting cyclic H3K4 trimethylation and recruitment of BMAL1 to chromatin.
2021-01-11 | GSE126851 | GEO
Project description:Mammalian circadian rhythms are based on coupled transcriptional-translational feedback loops driven by the transcription factors CLOCK and BMAL1. Chromatin remodeling mechanisms are essential for the proper timing and extent of circadian gene expression. We report that the S-adenosylhomocysteine (SAH) hydrolysing enzyme AHCY binds to CLOCK-BMAL1 at chromatin and drives circadian transcription by promoting cyclic H3K4 trimethylation and recruitment of BMAL1 to chromatin.
2020-02-01 | GSE125720 | GEO
Project description:The circadian clock tightly interacts with cellular metabolism, and nutritional challenges can profoundly remodel its function. Dietary methionine restriction has been shown to improve metabolic health and extend lifespan. However, whether and how dietary methionine restriction impacts the circadian clock is unclear. Here, we demonstrate that methionine deprivation (MD) induces dramatic alterations in two signaling systems that input to the circadian clock: de novo oscillation of circulating FGF21 coupled with increased amplitude of glucocorticoid oscillations. These alterations in signaling result in a remarkable reprogramming of the hepatic circadian transcriptome and epigenetic landscape. The epigenetic and transcriptomic alterations result from dramatic remodeling of the rhythmic binding of the glucocorticoid receptor (GR) to chromatin as they are abolished by liver-specific deletion of GR. These results demonstrate that dietary methionine restriction remodels the circadian rhythms alterations in the biological program initiated by glucocorticoid receptor.
2026-09-23 | GSE288647 | GEO
Project description:The circadian clock tightly interacts with cellular metabolism, and nutritional challenges can profoundly remodel its function. Dietary methionine restriction has been shown to improve metabolic health and extend lifespan. However, whether and how dietary methionine restriction impacts the circadian clock is unclear. Here, we demonstrate that methionine deprivation (MD) induces dramatic alterations in two signaling systems that input to the circadian clock: de novo oscillation of circulating FGF21 coupled with increased amplitude of glucocorticoid oscillations. These alterations in signaling result in a remarkable reprogramming of the hepatic circadian transcriptome and epigenetic landscape. The epigenetic and transcriptomic alterations result from dramatic remodeling of the rhythmic binding of the glucocorticoid receptor (GR) to chromatin as they are abolished by liver-specific deletion of GR. These results demonstrate that dietary methionine restriction remodels the circadian rhythms alterations in the biological program initiated by glucocorticoid receptor.
2026-09-23 | GSE288645 | GEO
Project description:The circadian clock tightly interacts with cellular metabolism, and nutritional challenges can profoundly remodel its function. Dietary methionine restriction has been shown to improve metabolic health and extend lifespan. However, whether and how dietary methionine restriction impacts the circadian clock is unclear. Here, we demonstrate that methionine deprivation (MD) induces dramatic alterations in two signaling systems that input to the circadian clock: de novo oscillation of circulating FGF21 coupled with increased amplitude of glucocorticoid oscillations. These alterations in signaling result in a remarkable reprogramming of the hepatic circadian transcriptome and epigenetic landscape. The epigenetic and transcriptomic alterations result from dramatic remodeling of the rhythmic binding of the glucocorticoid receptor (GR) to chromatin as they are abolished by liver-specific deletion of GR. These results demonstrate that dietary methionine restriction remodels the circadian rhythms alterations in the biological program initiated by glucocorticoid receptor.
2026-09-23 | GSE288644 | GEO
Project description:The circadian clock tightly interacts with cellular metabolism, and nutritional challenges can profoundly remodel its function. Dietary methionine restriction has been shown to improve metabolic health and extend lifespan. However, whether and how dietary methionine restriction impacts the circadian clock is unclear. Here, we demonstrate that methionine deprivation (MD) induces dramatic alterations in two signaling systems that input to the circadian clock: de novo oscillation of circulating FGF21 coupled with increased amplitude of glucocorticoid oscillations. These alterations in signaling result in a remarkable reprogramming of the hepatic circadian transcriptome and epigenetic landscape. The epigenetic and transcriptomic alterations result from dramatic remodeling of the rhythmic binding of the glucocorticoid receptor (GR) to chromatin as they are abolished by liver-specific deletion of GR. These results demonstrate that dietary methionine restriction remodels the circadian rhythms alterations in the biological program initiated by glucocorticoid receptor.
2026-09-23 | GSE288646 | GEO
Project description:We show that the cyclin-dependent kinase 5 (CDK5) regulates the mammalian circadian clock via phosphorylation of PER2. CDK5 phosphorylated PER2 at serine residue 394 (S394) as shown by an in vitro kinase assay.
2019-12-04 | PXD012068 | Pride