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Transcriptome changes in mouse livers upon Bmal1 or Nr1d1 knock out and interactome of lnc-Crot by 4C-seq

ABSTRACT: To explore the circadian regulations of Bmal1, we examined the transcriptome changes in mouse livers upon Bmal1 knock out at two circadian time points, CT0 and CT12. To explore the circadian regulations of Nr1d1, we examined the transcriptome changes in mouse livers upon Nr1d1 knock out at two circadian time points, CT0 and CT12. To explore interactome of lnc-Crot, 4C-seq was performed with lnc-Crot as bait region at CT6 and CT18.

ORGANISM(S): Mus musculus

PROVIDER: GSE87299 | GEO | 2017/04/12

SECONDARY ACCESSION(S): PRJNA344200

REPOSITORIES: GEO

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Transcriptome changes in mouse livers upon Bmal1 knock out

Project description:To explore the circadian regulations of Bmal1, we examined the transcriptome changes in mouse livers upon Bmal1 knock out at two circadian time points, CT0 and CT12.

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Transcriptomic changes following NR1D1 modulation in thyroid cancer cell lines

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2012-10-21 | E-GEOD-35026 | biostudies-arrayexpress

Mus musculus

Project description:Transcriptome changes in mouse livers upon Bmal1 or Nr1d1 knock out and interactome of lnc-Crot by 4C-seq

| PRJNA344200 | ENA

Zebrafish whole brain single cell RNA-seq of nr1d1:VNP fish

Project description:we report a transgenic zebrafish line using destabilized fluorescent protein, Venus-NLS-PEST (VNP), driven by the promoter of a key circadian clock gene, nr1d1. This system allows us to monitor the development of single-cell circadian rhythm in live zebrafish larva in a cell-type specific manner. To identify the cell types expressing nr1d1:VNP in the whole brain, we conducted single cell RNA-seq (scRNA-seq) of ~15,000 cells dissociated from the brain of Tg(nr1d1:VNP) larval fish at 6.5dpf. Among them, 6514 cells were identified with number of genes > 500 and used for the following analysis. 26 cells clusters were classified from scRNAseq, and manually annotated by comparing the marker genes with the adult zebrfiash whole brain single cell RNA-seq data. The mRNA of nr1d1:VNP was enriched in photoreceptors in pineal gland, granule cells and purkinje cells in cerebellum, habenula cells as well as non-neuron cell.

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Transcriptional Repressor Gm129 Modulates the Circadian Gene Expression by Inhibiting CLOCK:BMAL1 Activity

Project description:The mammalian circadian clock is a molecular oscillator composed of a feedback loop that involves transcriptional activators CLOCK and BMAL1, and repressors Cryptochrome (CRY) and Period (PER). Here we show that a direct CLOCK-BMAL1 target gene, Gm129, is a novel regulator of the feedback loop. ChIP analysis revealed that the CLOCK:BMAL1:CRY1 complex strongly occupies the promoter region of Gm129. Both mRNA and protein levels of GM129 exhibit high amplitude circadian oscillations in mouse liver, and Gm129 gene encodes a nuclear-localized protein that directly interacts with BMAL1 and represses CLOCK:BMAL1 activity. In vitro and in vivo protein-DNA interaction results demonstrate that, like CRY1, GM129 functions as a repressor by binding to the CLOCK:BMAL1 complex on DNA. Although Gm129-/- or Cry1-/- Gm129-/- mice retain a robust circadian rhythm, the peaks of Nr1d1 and Dbp mRNAs in liver exhibit significant phase delay compared to control. Our results suggest that, in addition to CRYs and PERs, GM129 protein contributes to the transcriptional feedback loop by modulating CLOCK:BMAL1 activity as a transcriptional repressor. Examination of 3 transcriptional regulators in mouse liver

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昼夜时钟蛋白NR1D1通过调节线粒体生物合成和脂质运输来控制颗粒细胞内分泌功能

Project description:With rapid economic and social development, people's living habits have changed dramatically. Long-term exposure to artificial light, shift work and staying up late have been found to seriously disrupt people's normal biological rhythms and impair female reproductive function, leading to increased rates of infertility and abortion. In this study, we established a mouse model of continuous light exposure to explore the effects of long-term environmental circadian disturbances on the reproductive endocrine function and related mechanisms in females. We found that continuous light exposure caused reproductive and endocrine metabolic abnormalities in female mice, including estrous cycle disorders, ovarian changes of increased unruptured luteinized cystic follicles, LH elevation and hyperandrogenism. Moreover, the circadian rhythm genes expression in follicular granulosa cells was disrupted, in particular the expression of Nr1d1 showed a significant increase at night. We further showed that the up-regulation of NR1D1 promoted the expression of mitochondrial biosynthesis protein PGC1α and lipid transport related proteins such as SLC27A6, CPT1α, etc, in granulosa cells, and activated the PTEN/PI3K/AKT signaling pathway, leading to premature luteinization of granulosa cells. In addition, the gap junctions between cumulus and oocytes were prematurely closed in COCs treated with NR1D1 agonist GSK4112, which impaired oocyte quality, resulting in reduced maturation, disordered spindle assembly and chromosome arrangement, mitochondrial dysfunction. In conclusion, the circadian clock protein NR1D1 plays an essential role in maintaining granulosa cell endocrine function and oocyte quality. The findings may provide fresh insights into how circadian rhythm disturbances caused by staying up late and continuous exposure to artificial light sources can damage female reproductive function.

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