Transcriptome analysis of Rev-erbs skeletal muscle specific knockout muscles and WT muscles
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1050255 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27155281_1.fastq.gz | Fastqsanger.gz | |||
| SRR27155281_2.fastq.gz | Fastqsanger.gz | |||
| SRR27155282_1.fastq.gz | Fastqsanger.gz | |||
| SRR27155282_2.fastq.gz | Fastqsanger.gz | |||
| SRR27155283_1.fastq.gz | Fastqsanger.gz |
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Project description:We used Rev-erbs skeletal muscle specific knockout mouse model to illustrate the Rev-erbs function in skeletal muscle. In this study, transcriptome sequencing was used to detect the mRNA expression profiles of KO muscles and WT muscles.
2025-05-04 | GSE249730 | GEO
Project description:Rev-erb plays a pivotal role in coordinating circadian rhythms and in regulating metabolism. However, The regulation of muscle metabolism by Rev-erbs is still not fully understood. In this study, we explored the mechanisms through which Rev-erb regulates skeletal muscle by using ChIP-seq.
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Project description:Skeletal muscle Rev-erbs regulates metabolic diurnal rhythm
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Project description:Rev-Erba and Rev-Erbb are nuclear receptors that regulate the expression of genes involved in the control of circadian rhythm, metabolism, and inflammatory responses. Rev-Erbs function as transcriptional repressors by recruiting NCoR/HDAC3 co-repressor complexes to Rev-Erb response elements in enhancers and promoters of target genes, but the molecular basis for cell-specific programs of repression is not known. Here, we present evidence that in macrophages, Rev-Erbs regulate target gene expression by inhibiting the functions of distal enhancers that are selected by macrophage lineage-determining factors, thereby establishing a macrophage-specific program of repression. Remarkably, the repressive functions of Rev-Erbs are associated with their ability to inhibit the transcription of enhancer-derived RNAs (eRNAs). Furthermore, targeted degradation of eRNAs at two enhancers subject to negative regulation by Rev-Erbs resulted in reduced expression of nearby mRNAs, implying a direct role of these eRNAs in enhancer function. By precisely defining eRNA start sites using a method that quantifies nascent 5' ends (5'-GRO-Seq), we show that transfer of full enhancer activity to a target promoter requires both the sequences mediating transcription factor binding and the specific sequences encoding the eRNA transcript. These studies provide evidence for direct roles of eRNAs in contributing to enhancer functions and suggest that Rev-Erbs act to suppress gene expression at a distance by repressing eRNA transcription. Using ChIPseq, GRO-seq, and 5'GRO-seq to determine mechanism of RevErb in transcriptional regulation in macrophages
2013-06-05 | E-GEOD-45914 | biostudies-arrayexpress
Project description:Rev-Erba and Rev-Erbb are nuclear receptors that regulate the expression of genes involved in the control of circadian rhythm, metabolism, and inflammatory responses. Rev-Erbs function as transcriptional repressors by recruiting NCoR/HDAC3 co-repressor complexes to Rev-Erb response elements in enhancers and promoters of target genes, but the molecular basis for cell-specific programs of repression is not known. Here, we present evidence that in macrophages, Rev-Erbs regulate target gene expression by inhibiting the functions of distal enhancers that are selected by macrophage lineage-determining factors, thereby establishing a macrophage-specific program of repression. Remarkably, the repressive functions of Rev-Erbs are associated with their ability to inhibit the transcription of enhancer-derived RNAs (eRNAs). Furthermore, targeted degradation of eRNAs at two enhancers subject to negative regulation by Rev-Erbs resulted in reduced expression of nearby mRNAs, implying a direct role of these eRNAs in enhancer function. By precisely defining eRNA start sites using a method that quantifies nascent 5' ends (5'-GRO-Seq), we show that transfer of full enhancer activity to a target promoter requires both the sequences mediating transcription factor binding and the specific sequences encoding the eRNA transcript. These studies provide evidence for direct roles of eRNAs in contributing to enhancer functions and suggest that Rev-Erbs act to suppress gene expression at a distance by repressing eRNA transcription.
2013-06-05 | GSE45914 | GEO
Project description:We mapped the genome-wide binding profiles of BMAL1 and REV-ERB⍺ during peak protein expression of each factor (ZT4, and ZT8, respectively) by ChIP-Seq in gastrocnemius muscles from control C57BL/6J mice.
2018-07-20 | GSE108650 | GEO
Project description:The nuclear receptors (NRs) REV-ERBα and β, encoded by Nr1d1 and Nr1d2, link circadian rhythms and metabolism. REV-ERB lacks the canonical NR activation domain, and thus functions as a transcriptional repressor. Like other NRs, REV-ERBs can be regulated by ligands, including naturally occurring heme, which potentiate their repressive activity. Attempts to pharmacologically target REV-ERBs by the use of putatively specific synthetic agonists, particularly SR90096, have suggested a wide range of beneficial effects in healthy as well as diseased animal models and cell systems. For instance, Sulli et al. recently reported that REV-ERB activation by SR9009 is specifically lethal to cancer (stem) cells but not other cell types. Because REV-ERBs are core components of the molecular clock, the results were interpreted as a link between the body’s circadian timekeeping system and cancer. Moreover, increased energy expenditure after SR9009 administration decreases obesity in mice, and the reported activity of SR9009 as an exercise mimetic in skeletal muscle have resulted in online sales of the compound as a performance-enhancing drug, with advertisements reassuringly highlighting REV-ERBs as the molecular target (https://www.evolutionary.org/stenabolic-sr9009-review; https://www.simplyanabolics.com/sarms/sr9009-stenabolic/).
2019-05-08 | GSE123312 | GEO
Project description:Neuropathic pain is one of the most intractable pain conditions associated with tumor growth compressing and damaging nerves. A troublesome hallmark symptom of neuropathic pain is hypersensitivity to innocuous stimuli, known as “tactile allodynia,” which is often refractory to currently available analgesics. Diurnal variations in pain hypersensitivity are common in patients with cancer, but the underlying mechanisms are enigmatic. Herein, we report that spinal expression of lipocalin-2 (LCN2) enhances pain sensitivity of NCTC2472 fibrosarcoma-implanted male mice during specific stages of the diurnal cycle. As the tumor grew, interleukin-6 (IL-6) levels increased in the spinal cord of the mice. Increased IL-6 levels stimulated LCN2 expression in spinal microglia, but this expression was periodically repressed by the circadian clock components REV-ERBα and REV-ERBβ. Notably, intra-spinal dorsal horn injection of lentiviral vectors expressing REV-ERBα or REV-ERBβ in tumor-bearing mice alleviated tactile allodynia. Furthermore, intrathecal injection of SR9009, a synthetic agonist of REV-ERBs, also attenuated cancer-induced pain hypersensitivity, accompanied by suppressing spinal LCN2 expression. These results suggest that temporal elevation of LCN2 expression decreases the threshold of tactile pain hypersensitivity induced by tumor growth. We propose that the circadian clock component of REV-ERBs is an effective target for alleviation of cancer-induced tactile allodynia, identifying a new class of analgesic agents.
2025-04-27 | GSE255355 | GEO
Project description:The circadian clock regulates behavioural and physiological processes in a 24-h cycle. The nuclear receptors REV-ERBa and REV-ERBb are involved in the cell-autonomous circadian transcriptional/translational feedback loops as transcriptional repressors. A number of studies have also demonstrated a pivotal role of REV-ERBs in regulation of metabolic, neuronal, and inflammatory functions including bile acid metabolism, lipid metabolism, and production of inflammatory cytokines. Given the multifunctional role of REV-ERBs, it is important to elucidate the mechanism through which REV-ERBs exert their functions. To this end, we established a Rev-erba/Rev-erbb double-knockout mouse embryonic stem (ES) cell model and analyzed the circadian clock and clock-controlled output gene expressions. A comprehensive mRNA-seq analysis revealed that the complete knockout of both Rev-erba and Rev-erbb does not abrogate expression rhythms of E-box-regulated core clock genes but drastically changes a diverse set of other rhythmically-expressed output genes. Of note, REV-ERBa/b deficiency does not compromise circadian expression rhythms of PER2, while REV-ERB target genes, Bmal1 and Npas2, are significantly upregulated. This study emphasizes REV-ERBs function to form an essential link between the circadian clock and a wide variety of cellular physiological functions.
2019-07-29 | GSE125696 | GEO
Project description:Obesity occurs when energy expenditure is outweighed by food intake. Tuberal hypothalamic nuclei, including the arcuate nucleus (ARC), ventromedial nucleus (VMH), and dorsomedial nucleus (DMH), regulate feeding amount as well as energy expenditure. Here we report that mice lacking circadian nuclear receptors REV-ERBa and b in the tuberal hypothalamus (HDKO) gain excessive weight on an obesogenic diet due both to decreased energy expenditure and increased food consumption during the light phase. Moreover, rebound food intake after fasting is markedly increased in HDKO mice. Integrative transcriptomic and cistromic analyses revealed that such disruption in feeding behavior is due to perturbed REV-ERB-dependent leptin signaling in the ARC. Indeed, in vivo leptin sensitivity is impaired in HDKO mice on an obesogenic diet in a circadian manner. Thus, REV-ERBs play a crucial role in hypothalamic regulation of food intake and circadian leptin sensitivity in diet-induced obesity.
2020-10-11 | GSE148641 | GEO