HepG2 Hi-C
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE113405 | GEO | 2018/10/08
REPOSITORIES: GEO
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Project description:Partially methylated domains are extended regions in the genome exhibiting a reduced average DNA methylation level. They cover gene poor and transcriptionally inactive regions and tend to be heterochromatic. We present a comprehensive comparative analysis of partially methylated domains in human and mouse cells, to identify structural and functional features associated with them.
| EGAS00001003157 | EGA
Project description:We carry out whole-genome bisulfite sequencing (WGBS) of rat placental DNA to investigate epigenome-wide alterations in a reduced uterine perfusion pressure (RUPP) PE model. The Hidden Markov Model (HMM) was applied to identify functional epigenetic structures including partially methylated domains (PMDs), low methylated regions (LMRs) and unmethylated regions (UMRs).
2023-08-12 | GSE211194 | GEO
Project description:DNA methylation is essential for embryonic and neuronal differentiation, but the function of most genomic DNA methylation marks are poorly understood. Generally the human genome is highly methylated (>70%) except for CpG islands and gene promoters. However, it was recently shown that the IMR90 human fetal lung fibroblast cells have large regions of the genome with partially methylated domains (PMDs, <70% average methylation), in contrast to the rest of the genome which is in highly methylated domains (HMDs, >70% average methylation). Using bisulfite conversion followed by high-throughput sequencing (MethylC-seq), we discovered that human SH-SY5Y neuronal cells also contain PMDs. We developed a novel hidden Markov model (HMM) to computationally map the genomic locations of PMDs in both cell types and found that autosomal PMDs can be over 9 Mb in length and cover 41% of the IMR90 genome and 19% of the SH-SY5Y genome. Genomic regions marked by cell line specific PMDs contain genes that are expressed in a tissue-specific manner, with PMDs being a mark of repressed transcription. Genes contained within N-HMDs (neuronal HMDs, defined as a PMD in IMR90 but HMD in SH-SY5Y) were significantly enriched for calcium signaling, synaptic transmission and neuron differentiation functions. Autism candidate genes were enriched within PMDs and the largest PMD observed in SH-SY5Y cells marked a 10 Mb cluster of cadherin genes with strong genetic association to autism. Our results suggest that these large-scale methylation domain maps could be relevant to interpreting and directing future investigations into the elusive etiology of autism. Examined DNA methylation in a human neuronal cell line and cerebral cortex
2011-06-23 | E-GEOD-25930 | biostudies-arrayexpress
Project description:Examination of two DNA methylomes at the most extreme points of their lives to see differences that might contribute to explain the aged phenotype We have performed Whole Genome Bisulfite Sequencing (WGBS) and methylation array technology of newborn and a centenarian samples to address the Epigenetic drifts in Human aging, which might be an alternative pathway to explain the age-associated alterations. In addition, we used SNP array platforms to exclude an influence of copy number changes with age and SNPs on the identification of differentially methylated regions. This Series represents the methylation array data. The WGBS data are available in GSE31263.
2012-07-10 | E-GEOD-31438 | biostudies-arrayexpress
Project description:DNA methylation is essential for embryonic and neuronal differentiation, but the function of most genomic DNA methylation marks are poorly understood. Generally the human genome is highly methylated (>70%) except for CpG islands and gene promoters. However, it was recently shown that the IMR90 human fetal lung fibroblast cells have large regions of the genome with partially methylated domains (PMDs, <70% average methylation), in contrast to the rest of the genome which is in highly methylated domains (HMDs, >70% average methylation). Using bisulfite conversion followed by high-throughput sequencing (MethylC-seq), we discovered that human SH-SY5Y neuronal cells also contain PMDs. We developed a novel hidden Markov model (HMM) to computationally map the genomic locations of PMDs in both cell types and found that autosomal PMDs can be over 9 Mb in length and cover 41% of the IMR90 genome and 19% of the SH-SY5Y genome. Genomic regions marked by cell line specific PMDs contain genes that are expressed in a tissue-specific manner, with PMDs being a mark of repressed transcription. Genes contained within N-HMDs (neuronal HMDs, defined as a PMD in IMR90 but HMD in SH-SY5Y) were significantly enriched for calcium signaling, synaptic transmission and neuron differentiation functions. Autism candidate genes were enriched within PMDs and the largest PMD observed in SH-SY5Y cells marked a 10 Mb cluster of cadherin genes with strong genetic association to autism. Our results suggest that these large-scale methylation domain maps could be relevant to interpreting and directing future investigations into the elusive etiology of autism.
2011-06-23 | GSE25930 | GEO
Project description:As one of the most common malignancies, esophageal cancer has two subtypes, squamous cell carcinoma (ESCC) and adenocarcinoma (EAC), arising from distinct cells-of-origin. However, distinguishing cell-type-specific molecular features from cancer-specific characteristics has been challenging. Here, we analyze whole-genome bisulfite sequencing (WGBS) data on 45 esophageal tumor and nonmalignant samples from both subtypes. We develop a novel sequence-aware method to identify large partially methylated domains (PMDs), revealing profound heterogeneity at both the methylation level (depth) and genomic distribution (breadth) of PMDs across tumor samples. We identify subtype-specific PMDs, which are associated with repressive transcription, chromatin B compartments and high somatic mutation rate. While the genomic locations of these PMDs are pre-established in normal cells, the degree of loss is significantly higher in tumors. We find that cell-type-specific deposition of H3K36me2 may underlie the genomic distribution PMDs. At a smaller genomic scale, both cell-type- and cancer-specific differentially methylated regions (DMRs) are identified for each subtype. Using binding motif analysis within these DMRs, we show that a cell-type-specific transcription factor such as HNF4A can maintain the binding sites that it establishes in normal cells, while being recruited to new binding sites with novel partners such as FOSL1 in cancer. Finally, leveraging pan-tissue single-cell and pan-cancer epigenomic datasets, we demonstrate that a substantial fraction of the cell-type-specific PMDs and DMRs identified here in esophageal cancer, are actually markers that co-occur in other cancers originating from related cell types. These findings advance our understanding of the DNA methylation dynamics at various genomic scales in normal and malignant states, providing novel mechanistic insights into cell-type- and cancer-specific epigenetic regulations. Whole-genome bisulfite sequencing (WGBS) for EAC ESO26 cell line and ESCC TE5 cell line.
2023-08-04 | GSE210218 | GEO
Project description:Medaka sperm methylomes were sequenced using whole genome bisulfite sequencing (WGBS)
2019-04-23 | GSE128797 | GEO
Project description:Medaka PGCs methylomes were sequenced using whole genome bisulfite sequencing (WGBS)
2019-12-25 | GSE130002 | GEO
Project description:We used single-cell WGBS to profile DNA methylomes of human oocytes at different maturation stages
2017-06-23 | GSE71985 | GEO
Project description:Chromosomes must correctly fold in eukaryotic nuclei for proper genome function. Eukaryotic organisms hierarchically organize their genomes: in the fungus Neurospora crassa, chromatin fiber loops compact into Topologically Associated Domain (TAD)-like structures that are anchored by heterochromatic region aggregates. However, insufficient information exists on how histone post-translational modifications, including acetylation, impact genome organization. In Neurospora, the HCHC (HDA-1, CDP-2, HP1, CHAP) complex deacetylates heterochromatic regions including centromeres: loss of individual HCHC members increases centromeric acetylation and cytosine methylation. Here, we evaluate the role of the HCHC complex on genome organization using chromosome conformation capture with high-throughput sequencing (Hi-C) in Δcdp-2 or Δchap deletion strains. CDP-2 loss increases interactions between intra- and inter-chromosomal heterochromatic regions, while removal of CHAP decreases heterochromatic region compaction. Individual HCHC mutants exhibit different histone PTM patterns genome-wide: in Dcdp-2, heterochromatic H4K16 acetylation is increased, yet some heterochromatic regions lose H3K9 trimethylation, which locally increases inter-heterochromatin contacts; CHAP loss produces minimal acetylation changes but increases H3K9me3 enrichment in heterochromatin. Furthermore, deletion of the DIM-2 DNA methyltransferase in a Δcdp-2 background causes extensive genome disorder, as heterochromatic-euchromatic contacts increase despite additional H3K9me3 enrichment. Our results highlight how enhanced cytosine methylation ensures heterochromatic compartmentalization when silenced regions are acetylated.
2023-07-03 | GSE232934 | GEO