Characterization of tissue-specific BMAL1 cistromes reveals new roles for enhancer-enhancer interactions in regulating rhythmic transcription [ChIA-PET]
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ABSTRACT:
PROVIDER: PRJNA434105 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6726390.fastq.gz | Fastqsanger.gz | |||
| SRR6726391.fastq.gz | Fastqsanger.gz | |||
| SRR6726392.fastq.gz | Fastqsanger.gz | |||
| SRR6726393.fastq.gz | Fastqsanger.gz | |||
| SRR6726394.fastq.gz | Fastqsanger.gz |
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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 | GSE110603 | GEO
Project description:The mammalian circadian clock relies on the transcription factor CLOCK:BMAL1 to coordinate the rhythmic expression of thousands of genes. Consistent with the various biological functions under clock control, rhythmic gene expression is tissue-specific despite an identical clockwork mechanism in every cell. Here we show that BMAL1 DNA binding is largely tissue-specific, likely because of differences in chromatin accessibility between tissues and cobinding of tissue-specific transcription factors. Our results also indicate that BMAL1 ability to drive tissue-specific rhythmic transcription is associated with not only the activity of BMAL1-bound enhancers but also the activity of neighboring enhancers. Characterization of physical interactions between BMAL1 enhancers and other cis-regulatory regions by RNA polymerase II chromatin interaction analysis by paired-end tag (ChIA-PET) reveals that rhythmic BMAL1 target gene expression correlates with rhythmic chromatin interactions. These data thus support that much of BMAL1 target gene transcription depends on BMAL1 capacity to rhythmically regulate a network of enhancers.
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Project description:Characterization of tissue-specific BMAL1 cistromes reveals new roles for enhancer-enhancer interactions in regulating rhythmic transcription
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Project description:The pluripotent state of embryonic stem cells (ESCs) is produced by active transcription of cell identity genes and repression of genes encoding lineage-specifying developmental regulators. Here we use large ESC cohesin ChIA-PET datasets and other genomic data to identify the local chromosomal structures at both active and repressed genes across the genome. The results show that super-enhancer driven cell identity genes generally occur within large loops that are connected through CTCF-CTCF interaction sites occupied by cohesin. Smc1 ChIA-PET data from wild type murine embryonic stem cells V6.5 were generated by deep sequencing using Illumina Hi-Seq 2000.
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Project description:Genome-wide rhythmic occupancy of RNA polymerase II (RNAPII) is highly coordinated with rhythmic genes expression. Rhythmic RNAPII binding dynamically modulates diurnal 3D genome architecture remodeling with 91% of the chromatin interactions were altered. The rhythmic genes cluster at the 8:00 (AM) circadian phase form spatial interacting clusters in turn assist coordinated rhythmic gene expression, while non-rhythmic genes tend to tether together and contribute to expression at 20:00 (PM) circadian window. Target genes and associated cis-binding motifs of transcription factors enrichment points to the existence of subnuclear organization hub enriched around the TFs. RNAPII-associated chromatin interaction domains (CIDs) are under circadian control, and static CIDs with common node genes but changed connecting genes along the circadian cycle, reveal they may function as distinct clock components in the interconnected circuits between morning and evening. Core circadian clock genes related chromatin connectivity networks reveal a compact and highly connected chromatin architecture serving to coordinate gene expression in the morning, whereas a scattered, loose chromatin architecture coordinates PM gene expression. Our findings uncover novel diurnal fundamental genome folding principles in plants, and reveal the distinct higher-order chromosome organization that is crucial for coordinating diurnal dynamics of transcriptional regulation.
2021-12-24 | GSE143721 | GEO
Project description:RNA Polymerase II ChIA-PET data has revealed enhancers that are active in a profiled cell type and the genes that the enhancers regulate through chromatin interactions. The most commonly used computational method for analyzing ChIA-PET data, the ChIA-PET Tool, discovers interaction anchors at a spatial resolution that is insufficient to accurately identify individual enhancers. We introduce $Germ$, a computational method that estimates the likelihood that any two narrowly defined genomic locations are jointly occupied by RNA Polymerase II. $Germ$ takes a blind deconvolution approach to simultaneously estimate the likelihood of RNA Polymerase II occupation as well as a model of the arrangement of read alignments relative to locations occupied by RNA Polymerase II. Both types of information are utilized to estimate the likelihood that RNA Polymerase II jointly occupies any two genomic locations. We apply $Germ$ to RNA Polymerase II ChIA-PET data from embryonic stem cells to identify the genomic locations that are jointly occupied along with transcription start sites. We show that these genomic locations align more closely with features of active enhancers measured by ChIP-Seq than the locations identified using the ChIA-PET Tool. We also apply $Germ$ to RNA Polymerase II ChIA-PET data from motor neuron progenitors. Based on the $Germ$ results, we observe that a combination of cell type specific and cell type independent regulatory interactions are utilized by cells to regulate gene expression.
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Project description:The pluripotent state of embryonic stem cells (ESCs) is produced by active transcription of cell identity genes and repression of genes encoding lineage-specifying developmental regulators. Here we use large ESC cohesin ChIA-PET datasets and other genomic data to identify the local chromosomal structures at both active and repressed genes across the genome. The results show that super-enhancer driven cell identity genes generally occur within large loops that are connected through CTCF-CTCF interaction sites occupied by cohesin. H3K27me3 ChIP-seq data from wild type murine embryonic stem cells V6.5 were generated by deep sequencing using Illumina Hi-Seq 2000.
2014-06-27 | E-GEOD-57912 | biostudies-arrayexpress
Project description:This data was generated by ENCODE. If you have questions about the data, contact the submitting laboratory directly (Yijun Ruan mailto:ruanyj@gis.a-star.edu.sg). If you have questions about the Genome Browser track associated with this data, contact ENCODE (mailto:genome@soe.ucsc.edu). This track was produced as part of the ENCODE Project. It shows the locations of protein factor mediated chromatin interactions determined by Chromatin Interaction Analysis with Paired-End Tag (ChIA-PET) data (Fullwood et al., 2010) extracted from five different human cancer cell lines (K562 (chronic myeloid leukemia), HCT116 (colorectal cancer), HeLa-S3 (cervical cancer), MCF-7 (breast cancer), and NB4 (promyelocytic)). A chromatin interaction is defined as the association of two regions of the genome that are far apart in terms of genomic distance, but are spatially proximate to each other in the 3-dimensional cellular nucleus. Additionally, ChIA-PET experiments generate transcription factor binding sites. A binding site is defined as a region of the genome that is highly enriched by specific Chromatin ImmunoPrecipitation (ChIP) against a transcription factor, which indicates that the transcription factor binds specifically to this region. The protein factors displayed in the track include estrogen receptor alpha (ERa), RNA polymerase II (RNAPII), and CCCTC binding factor (CTCF). For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Chromatin interaction analysis with paired-end tag sequencing (ChIA-PET) is a global de novo high-throughput method for characterizing the 3-dimensional structure of chromatin in the nucleus. In the ChIA-PET protocol, samples were cross-linked and fragmented, then subjected to chromatin immunoprecipitation. The DNA fragments that were brought together by the chromatin interactions were then proximity-ligated. During this proximity-ligation step, the half-linkers (created by the fragmentation) containing flanking MmeI sites (type IIS restriction enzymes) were first ligated to the DNA fragments and then ligated to each other to form full linkers. Full linkers bridge either two ends of a self-circularized fragment, or two ends of two different chromatin fragments. The material was then reverse cross-linked, purified and digested with MmeI. MmeI cuts 20 base pairs away from its recognition site. Tag-linker-tag (paired-end tag, PET) constructs were sequenced by ultra-high-throughput methods (Illumina or SOLiD paired-end sequencing). ChIA-PET reads were processed with the ChIA-PET Tool (Li et al., 2010) by the following steps: linker filtering, short reads mapping, PET classification, binding site identification, and interaction cluster identification. The high-confidence binding sites and chromatin interaction clusters were reported. Chromatin interactions identified by ChIA-PET have been validated by 3C, ChIP-3C, 4C and DNA-FISH (Fullwood et al., 2009).
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