Interplay between Genetic Variation and Nutrition Challenge Controls Hepatic Diurnal Rhythms [ChIA-PET]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1169623 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Variation in diurnal rhythms contributes to the risk of multiple diseases, yet the genomic and epigenomic basis remains largely unknown. Here, we show that SNPs in enhancer and promoter regions genome-wide contribute to variations in human diurnal rhythms. Differential rhythmic gene expression and physiological responses to diet-induced obesity in mice with different genetic backgrounds are linked to time-dependent enhancer-promoter interactions (EPI) regulated by cis-regulatory SNPs and transcription factors (TFs) like ESRRγ. Hepatocyte-specific Esrrγ knockout alters rhythmic processes in liver, including triglyceride synthesis and lipid droplet formation, across mouse strains. Moreover, motifs of ESRRγ and other lipid metabolism-related TFs are enriched in individual-specific EPIs harboring SNPs to control rhythmic genes in patients with MAFLD. SNPs located in these sites are correlated with hepatic metabolic traits. Thus, SNPs and TFs interdependently form the genomic and epigenomic basis for diurnal rhythm variation, contributing to disease risk.
2025-08-25 | GSE278922 | GEO
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.
2014-06-27 | E-GEOD-57911 | biostudies-arrayexpress
Project description:ChIA-PET from HCT116 (ENCSR028AOM)
| PRJNA1210558 | ENA
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).
2012-07-19 | E-GEOD-39495 | biostudies-arrayexpress
Project description:Diurnal 3D genome organization remodeling orchestrates rhythmic gene expression in rice [ChIA-PET]
| PRJNA601445 | ENA
Project description:Variation in diurnal rhythms contributes to the risk of multiple diseases, yet the genomic and epigenomic basis remains largely unknown. Here, we show that SNPs in enhancer and promoter regions genome-wide contribute to variations in human diurnal rhythms. Differential rhythmic gene expression and physiological responses to diet-induced obesity in mice with different genetic backgrounds are linked to time-dependent enhancer-promoter interactions (EPI) regulated by cis-regulatory SNPs and transcription factors (TFs) like ESRRγ. Hepatocyte-specific Esrrγ knockout alters rhythmic processes in liver, including triglyceride synthesis and lipid droplet formation, across mouse strains. Moreover, motifs of ESRRγ and other lipid metabolism-related TFs are enriched in individual-specific EPIs harboring SNPs to control rhythmic genes in patients with MAFLD. SNPs located in these sites are correlated with hepatic metabolic traits. Thus, SNPs and TFs interdependently form the genomic and epigenomic basis for diurnal rhythm variation, contributing to disease risk.
2025-08-25 | GSE278921 | GEO
Project description:Variation in diurnal rhythms contributes to the risk of multiple diseases, yet the genomic and epigenomic basis remains largely unknown. Here, we show that SNPs in enhancer and promoter regions genome-wide contribute to variations in human diurnal rhythms. Differential rhythmic gene expression and physiological responses to diet-induced obesity in mice with different genetic backgrounds are linked to time-dependent enhancer-promoter interactions (EPI) regulated by cis-regulatory SNPs and transcription factors (TFs) like ESRRγ. Hepatocyte-specific Esrrγ knockout alters rhythmic processes in liver, including triglyceride synthesis and lipid droplet formation, across mouse strains. Moreover, motifs of ESRRγ and other lipid metabolism-related TFs are enriched in individual-specific EPIs harboring SNPs to control rhythmic genes in patients with MAFLD. SNPs located in these sites are correlated with hepatic metabolic traits. Thus, SNPs and TFs interdependently form the genomic and epigenomic basis for diurnal rhythm variation, contributing to disease risk.
2025-08-25 | GSE278920 | GEO
Project description:Variation in diurnal rhythms contributes to the risk of multiple diseases, yet the genomic and epigenomic basis remains largely unknown. Here, we show that SNPs in enhancer and promoter regions genome-wide contribute to variations in human diurnal rhythms. Differential rhythmic gene expression and physiological responses to diet-induced obesity in mice with different genetic backgrounds are linked to time-dependent enhancer-promoter interactions (EPI) regulated by cis-regulatory SNPs and transcription factors (TFs) like ESRRγ. Hepatocyte-specific Esrrγ knockout alters rhythmic processes in liver, including triglyceride synthesis and lipid droplet formation, across mouse strains. Moreover, motifs of ESRRγ and other lipid metabolism-related TFs are enriched in individual-specific EPIs harboring SNPs to control rhythmic genes in patients with MAFLD. SNPs located in these sites are correlated with hepatic metabolic traits. Thus, SNPs and TFs interdependently form the genomic and epigenomic basis for diurnal rhythm variation, contributing to disease risk.
2025-08-25 | GSE297115 | GEO
Project description:Interplay between Genetic Variation and Nutrition Challenge Controls Hepatic Diurnal Rhythms [ATAC-seq]
| PRJNA1262740 | ENA
Project description:Interplay between Genetic Variation and Nutrition Challenge Controls Hepatic Diurnal Rhythms [RNA-seq]
| PRJNA1169622 | ENA