Identification of Bmal1 binding sites by ChIP-seq in mouse lung tissue
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB24363 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2241561_1.fastq.gz | Fastqsanger.gz | |||
| ERR2241561_2.fastq.gz | Fastqsanger.gz | |||
| ERR2241562_1.fastq.gz | Fastqsanger.gz | |||
| ERR2241562_2.fastq.gz | Fastqsanger.gz |
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Project description:Bmal1 ChIP-seq on C57/BL adult mouse lung tissue at Zeitgeber time ZT5.
2019-10-17 | E-MTAB-6354 | biostudies-arrayexpress
Project description:Using chromatin immuno-precipitation (ChIP) combined with deep sequencing (ChIP-seq) we obtained a time resolved and genome-wide map of BMAL1 binding in mouse liver, which allowed to identify over two thousand binding sites with peak binding narrowly centered around Zeitgeber time (ZT) 6. Annotation of BMAL1 targets confirms carbohydrate and lipid metabolism as the major output of the circadian clock in mouse liver. Moreover, transcription regulators are largely overrepresented, several of which also exhibit circadian activity. Genes of the core circadian oscillator stand out as strongly bound, often at promoter and distal sites. Genomic sequence analysis of the sites identified E- boxes and tandem E1-E2 consensus elements. Electromobility shift assays (EMSA) showed that E1-E2 sites are bound by a dimer of BMAL1/CLOCK heterodimers with a spacing-dependent cooperative interaction that was further validated in transactivation assays. BMAL1 target genes showed cyclic mRNA expression profiles with a phase distribution centered at ZT10. Importantly, sites with E1-E2 elements showed tighter phases both in binding and mRNA accumulation. Finally, comparing the temporal accumulation of precursor mRNA and mature mRNA helped distinguish direct BMAL1 targets from targets with more complex regulation, and showed how transcriptional and post-transcriptional regulation contribute differentially to circadian expression phase. Together, our analysis of a dynamic protein-DNA interactome uncovered how genes of the core circadian oscillator are wired together and drive phase-specific circadian output programs in a complex tissue. ChIP-Seq of BMAL1 in mouse liver during one circadian cycle at 4 hour time resolution presented in this Series (GSE26602). mRNA profiling data used in this study are already published (Kornmann et al, PLoS Biol 2007) and have been deposited on ArrayExpress repository (accession number: E-MEXP-842).
2011-02-23 | E-GEOD-26602 | biostudies-arrayexpress
Project description:Advances in circadian research revealed an intricate relationship between aging and circadian rhythms. However, whether and how the circadian machinery contribute to stem cell aging, especially in primates, remains poorly understood. In this study, we investigated the role of BMAL1, the only non-redundant circadian clock component, during aging in mesenchymal progenitor cells (MPCs). We observed an accelerated aging phenotype in both BMAL1 deficient human and cynomolgus monkey MPCs. Notably, this phenotype is mainly attributed to a transcriptional-independent role of BMAL1 in stabilizing the heterochromatin and thus preventing LINE1 activation. In senescent MPCs from human and cynomolgus monkeys, dampened LINE1 binding capacity of BMAL1 and synergistically activated LINE1 transcripts were observed. Furthermore, similar de-stabilized heterochromatin and aberrant LINE1s transcription was observed in the skin and muscle tissues from BMAL1-deficient cynomolgus monkey. Altogether, these findings uncover a noncanonical role of BMAL1 in stabilizing heterochromatin to inactivate LINE1 that drives aging in primates.
2022-03-18 | PXD030570 | Pride
Project description:The goal of this study was to define the binding sites of the core circadian factors, BMAL1 and CLOCK across the genome in adult mouse skeletal muscle. We found that mitochondrial inner-membrane genes were among the most enriched rhythmic genes via gene ontology analysis, and ChIP-Seq analysis corroborated the role of Clock and Bmal1 in targeting promoters of mitochondrial inner-membrane genes.
2021-08-12 | GSE143334 | GEO
Project description:Using chromatin immuno-precipitation (ChIP) combined with deep sequencing (ChIP-seq) we obtained a time resolved and genome-wide map of BMAL1 binding in mouse liver, which allowed to identify over two thousand binding sites with peak binding narrowly centered around Zeitgeber time (ZT) 6. Annotation of BMAL1 targets confirms carbohydrate and lipid metabolism as the major output of the circadian clock in mouse liver. Moreover, transcription regulators are largely overrepresented, several of which also exhibit circadian activity. Genes of the core circadian oscillator stand out as strongly bound, often at promoter and distal sites. Genomic sequence analysis of the sites identified E- boxes and tandem E1-E2 consensus elements. Electromobility shift assays (EMSA) showed that E1-E2 sites are bound by a dimer of BMAL1/CLOCK heterodimers with a spacing-dependent cooperative interaction that was further validated in transactivation assays. BMAL1 target genes showed cyclic mRNA expression profiles with a phase distribution centered at ZT10. Importantly, sites with E1-E2 elements showed tighter phases both in binding and mRNA accumulation. Finally, comparing the temporal accumulation of precursor mRNA and mature mRNA helped distinguish direct BMAL1 targets from targets with more complex regulation, and showed how transcriptional and post-transcriptional regulation contribute differentially to circadian expression phase. Together, our analysis of a dynamic protein-DNA interactome uncovered how genes of the core circadian oscillator are wired together and drive phase-specific circadian output programs in a complex tissue.
2011-02-23 | GSE26602 | GEO
Project description:Discovery of SOX2 binding sites in lung cancer cells by CHIPseq and validate the target genes in two lung cancer cells by CHIP-QPCR.
2020-04-10 | GSE97574 | GEO
Project description:Mouse livers were collected at 4 hours interval at constant darkness condition after 2 weeks synchronization to ambient light dark cycle, then conducted for the ChIP-seq (Bmal1, Ruvbl2). We found Ruvbl2 rhythmically co-occupancies with Bmal1 binding sites.
2020-05-07 | GSE130505 | GEO
Project description:We use PER2-inducible system to analyse BMAL1 chromatin binding by ChIPseq and expression profile by mRNA-Seq. PER2 decrease BMAL1 chromatin bindging but the effect on transcrtipion is gene-specific.
2017-01-10 | GSE93318 | GEO
Project description:The mammalian circadian clock relies on the transcription factor CLOCK:BMAL1 to coordinate the rhythmic expression of thousands of genes and enable biological functions to anticipate the daily environmental variations. Consistent with the wide range of biological functions under clock control, rhythmic gene expression is tissue-specific, and this even if the clockwork mechanism is identical in every cell. Here we show that BMAL1 DNA binding is largely tissue-specific, through mechanisms involving differences in chromatin accessibility between tissues as well as co-binding of tissue-specific transcription factors. Our results also indicate that the ability of BMAL1 to drive tissue-specific rhythmic transcription not only relies on the activity of BMAL1 cis-regulatory elements (CREs), but also on the activity of neighboring CREs. Characterization of the physical interactions between BMAL1 CREs and other CREs by RNA Polymerase II ChIA-PET in the mouse liver reveals that most interactions are stable over the course of the day, and suggests that BMAL1-mediated rhythmic transcription relies on its ability to regulate the transcriptional activity of other CREs. Our data therefore suggest that much of BMAL1 target gene transcription depends on BMAL1 capacity at rhythmically regulating a network of enhancers.
2018-05-08 | GSE110602 | GEO
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