Ontology highlight
ABSTRACT:
PROVIDER: PRJNA138555 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE27518: LATE-REPLICATING HETEROCHROMATIN IS CHARACTERISED BY DECREASED CYTOSINE METHYLATION IN THE HUMAN GENOME (expression) GSE27537: LATE-REPLICATING HETEROCHROMATIN IS CHARACTERISED BY DECREASED CYTOSINE METHYLATION IN THE HUMAN GENOME (HELP assay) Refer to individual Series
2011-08-05 | E-GEOD-27538 | biostudies-arrayexpress
Project description:LATE-REPLICATING HETEROCHROMATIN IS CHARACTERISED BY DECREASED CYTOSINE METHYLATION IN THE HUMAN GENOME (expression)
| PRJNA141863 | ENA
Project description:LATE-REPLICATING HETEROCHROMATIN IS CHARACTERISED BY DECREASED CYTOSINE METHYLATION IN THE HUMAN GENOME (HELP assay)
| PRJNA141861 | ENA
Project description:Heterochromatin is believed to be associated with increased levels of cytosine methylation. With the recent availability of genome-wide, high-resolution molecular data reflecting cytosine methylation or heterochromatic organization, such relationships can be explored systematically. As a well-defined surrogate for heterochromatin, we tested the relationship between DNA replication timing and cytosine methylation in two human cell types, unexpectedly finding that the later-replicating, more heterochromatic regions to be less methylated than early-replicating regions. When we integrated gene expression data into the study, we found that regions of increased gene expression were earlier replicating, as previously identified, and that transcription-targeted cytosine methylation (TTCM) in gene bodies accounts for the positive correlation with early replication. A Self-Organising Map (SOM) approach was able to identify genomic regions with early replication and increased methylation but lacking annotated transcripts, which would have been missed in simple two variable analyses and may encode unrecognized intergenic transcripts. We conclude that the relationship of cytosine methylation with heterochromatin is not simple, and depends on whether the genomic context is tandemly-repetitive sequences often found near centromeres, which are known to be heterochromatic and methylated, or the remaining majority of the genome, where cytosine methylation is targeted preferentially to the transcriptionally-active, euchromatic compartment of the genome. comparison of human fibroblast and GM06690
2011-08-05 | E-GEOD-27518 | biostudies-arrayexpress
Project description:Heterochromatin is believed to be associated with increased levels of cytosine methylation. With the recent availability of genome-wide, high-resolution molecular data reflecting cytosine methylation or heterochromatic organization, such relationships can be explored systematically. As a well-defined surrogate for heterochromatin, we tested the relationship between DNA replication timing and cytosine methylation in two human cell types, unexpectedly finding that the later-replicating, more heterochromatic regions to be less methylated than early-replicating regions. When we integrated gene expression data into the study, we found that regions of increased gene expression were earlier replicating, as previously identified, and that transcription-targeted cytosine methylation (TTCM) in gene bodies accounts for the positive correlation with early replication. A Self-Organising Map (SOM) approach was able to identify genomic regions with early replication and increased methylation but lacking annotated transcripts, which would have been missed in simple two variable analyses and may encode unrecognized intergenic transcripts. We conclude that the relationship of cytosine methylation with heterochromatin is not simple, and depends on whether the genomic context is tandemly-repetitive sequences often found near centromeres, which are known to be heterochromatic and methylated, or the remaining majority of the genome, where cytosine methylation is targeted preferentially to the transcriptionally-active, euchromatic compartment of the genome.
2011-08-06 | GSE27537 | GEO
Project description:Heterochromatin is believed to be associated with increased levels of cytosine methylation. With the recent availability of genome-wide, high-resolution molecular data reflecting cytosine methylation or heterochromatic organization, such relationships can be explored systematically. As a well-defined surrogate for heterochromatin, we tested the relationship between DNA replication timing and cytosine methylation in two human cell types, unexpectedly finding that the later-replicating, more heterochromatic regions to be less methylated than early-replicating regions. When we integrated gene expression data into the study, we found that regions of increased gene expression were earlier replicating, as previously identified, and that transcription-targeted cytosine methylation (TTCM) in gene bodies accounts for the positive correlation with early replication. A Self-Organising Map (SOM) approach was able to identify genomic regions with early replication and increased methylation but lacking annotated transcripts, which would have been missed in simple two variable analyses and may encode unrecognized intergenic transcripts. We conclude that the relationship of cytosine methylation with heterochromatin is not simple, and depends on whether the genomic context is tandemly-repetitive sequences often found near centromeres, which are known to be heterochromatic and methylated, or the remaining majority of the genome, where cytosine methylation is targeted preferentially to the transcriptionally-active, euchromatic compartment of the genome.
2011-08-06 | GSE27518 | GEO
Project description:DNA replication timing is known to facilitate the establishment of the epigenome, however, the intimate connection between replication timing and changes to the genome and epigenome in cancer remain largely uncharacterised. Here, we perform Repli-Seq and integrated epigenome analyses and demonstrate that genomic regions that undergo long-range epigenetic deregulation in prostate cancer also show concordant differences in replication timing. A subset of altered replication timing domains are conserved across cancers from different tissue origins. Notably, late-replicating regions in cancer cells display a loss of DNA methylation, and a switch in heterochromatin features from H3K9me3-marked constitutive to H3K27me3-marked facultative heterochromatin. Finally, analysis of 214 prostate and 35 breast cancer genomes reveal that late-replicating regions are prone to cis and early-replication to trans chromosomal rearrangements. Together, our data suggests that the nature of chromosomal rearrangement in cancer is related to the spatial and temporal positioning and altered epigenetic states of early-replicating compared to late-replicating loci.
2019-01-23 | GSE98730 | GEO
Project description:DNA replication timing is known to facilitate the establishment of the epigenome, however, the intimate connection between replication timing and changes to the genome and epigenome in cancer remain largely uncharacterised. Here, we perform Repli-Seq and integrated epigenome analyses and demonstrate that genomic regions that undergo long-range epigenetic deregulation in prostate cancer also show concordant differences in replication timing. A subset of altered replication timing domains are conserved across cancers from different tissue origins. Notably, late-replicating regions in cancer cells display a loss of DNA methylation, and a switch in heterochromatin features from H3K9me3-marked constitutive to H3K27me3-marked facultative heterochromatin. Finally, analysis of 214 prostate and 35 breast cancer genomes reveal that late-replicating regions are prone to cis and early-replication to trans chromosomal rearrangements. Together, our data suggests that the nature of chromosomal rearrangement in cancer is related to the spatial and temporal positioning and altered epigenetic states of early-replicating compared to late-replicating loci.
2019-01-23 | GSE98714 | GEO
Project description:DNA replication timing is known to facilitate the establishment of the epigenome, however, the intimate connection between replication timing and changes to the genome and epigenome in cancer remain largely uncharacterised. Here, we perform Repli-Seq and integrated epigenome analyses and demonstrate that genomic regions that undergo long-range epigenetic deregulation in prostate cancer also show concordant differences in replication timing. A subset of altered replication timing domains are conserved across cancers from different tissue origins. Notably, late-replicating regions in cancer cells display a loss of DNA methylation, and a switch in heterochromatin features from H3K9me3-marked constitutive to H3K27me3-marked facultative heterochromatin. Finally, analysis of 214 prostate and 35 breast cancer genomes reveal that late-replicating regions are prone to cis and early-replication to trans chromosomal rearrangements. Together, our data suggests that the nature of chromosomal rearrangement in cancer is related to the spatial and temporal positioning and altered epigenetic states of early-replicating compared to late-replicating loci.
2019-01-23 | GSE124274 | GEO
Project description:<p>Base mutations occur at higher frequencies within heterochromatin and late-replicating DNA. In this study, we show that regional differences in mutation frequency are absent in portions of the genome that are not transcribed within cutaneous squamous cell carcinomas (cSCCs) with an XPC-\- genetic background. The XPC-\- genetic background predicates a loss of global genome nucleotide excision repair (GG-NER), thus our data shows that regional differences in mutation frequency are a result of differential access of DNA repair protein. Unexpectedly, we also note that greater transcription reduces mutations on both strands of genes in heterochromatin, and only to those levels observed in euchromatin, in a XPC-dependent fashion. Therefore, transcription likely reduces mutation prevalence by increasing access to DNA repair proteins. This tripartite relationship between DNA repair, transcription, and chromatin state shows a new cancer risk factor in human populations.</p>
| phs000830 | dbGaP