Ontology highlight
ABSTRACT:
PROVIDER: PRJNA855483 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19973816_1.fastq.gz | Fastqsanger.gz | |||
| SRR19973816_2.fastq.gz | Fastqsanger.gz | |||
| SRR19973817_1.fastq.gz | Fastqsanger.gz | |||
| SRR19973817_2.fastq.gz | Fastqsanger.gz | |||
| SRR19973818_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 112 |
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Project description:Evolutionary causes and consequences of transponsable elements' epigenetic effects
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Project description:We study the relatively unexplored evolutionary consequences of the epigenetic effects of transpoable elements (TEs) by providing the first genome-wide quantification of such effects in wild-derived D. melanogaster and D. simulans strains. Surprisingly, over half of euchromatic TEs show spread of repressive epigenetic marks to nearby DNA, resulting in differential epigenetic states of homologous genic alleles and, in return, selection against TEs. Interestingly, compared to D. melanogaster, the lower TE content in D. simulans is correlated with stronger epigenetic effects of TEs and higher levels of host genetic factors known to promote epigenetic silencing. We conclude that the epigenetic effects of euchromatic TEs, and host genetic factors modulating such effects, play a critical role in the population dynamics of TEs within and between species.
2017-07-01 | GSE94735 | GEO
Project description:We study the relatively unexplored evolutionary consequences of the epigenetic effects of transpoable elements (TEs) by providing the first genome-wide quantification of such effects in wild-derived D. melanogaster and D. simulans strains. Surprisingly, over half of euchromatic TEs show spread of repressive epigenetic marks to nearby DNA, resulting in differential epigenetic states of homologous genic alleles and, in return, selection against TEs. Interestingly, compared to D. melanogaster, the lower TE content in D. simulans is correlated with stronger epigenetic effects of TEs and higher levels of host genetic factors known to promote epigenetic silencing. We conclude that the epigenetic effects of euchromatic TEs, and host genetic factors modulating such effects, play a critical role in the population dynamics of TEs within and between species.
2017-07-01 | GSE94741 | GEO
Project description:DNA methylation is an essential epigenetic modification, present in both unique DNA sequences and repetitive elements, but its exact function in repetitive elements remains obscure. Here, we describe the genome-wide comparative analysis of the 5mC, 5hmC, 5fC and 5caC profiles of repetitive elements in mouse embryonic fibroblasts and mouse embryonic stem cells. We provide evidence for distinct and highly specific DNA methylation/oxidation patterns of the repetitive elements in both cell types, which mainly affect CA repeats and evolutionary conserved mouse-specific transposable elements including IAP-LTRs, SINEs B1m/B2m and L1Md-LINEs. DNA methylation controls the expression of these retro-elements, which are clustered at specific locations in the mouse genome. We show that TDG is implicated in the regulation of their unique DNA methylation/oxidation signatures and their dynamics. Our data suggest the existence of novel epigenetic code for the most recently acquired evolutionary conserved repeats that could play a major role in cell differentiation. This SuperSeries is composed of the SubSeries listed below.
2017-02-22 | GSE66438 | GEO
Project description:DNA methylation is an essential epigenetic modification, present in both unique DNA sequences and repetitive elements, but its exact function in repetitive elements remains obscure. Here, we describe the genome-wide comparative analysis of the 5mC, 5hmC, 5fC and 5caC profiles of repetitive elements in mouse embryonic fibroblasts and mouse embryonic stem cells. We provide evidence for distinct and highly specific DNA methylation/oxidation patterns of the repetitive elements in both cell types, which mainly affect CA repeats and evolutionary conserved mouse-specific transposable elements including IAP-LTRs, SINEs B1m/B2m and L1Md-LINEs. DNA methylation controls the expression of these retro-elements, which are clustered at specific locations in the mouse genome. We show that TDG is implicated in the regulation of their unique DNA methylation/oxidation signatures and their dynamics. Our data suggest the existence of novel epigenetic code for the most recently acquired evolutionary conserved repeats that could play a major role in cell differentiation.
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Project description:An integrative genomic approach illuminates the causes and consequences of genetic background effects
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Project description:The relationship between evolutionary genome remodeling and the three-dimensional structure of the genome remain largely unexplored. Here we use the heavily rearranged gibbon genome to examine how evolutionary chromosomal rearrangements impact genome-wide chromatin interactions, topologically associating domains (TADs), and their epigenetic landscape. We use high-resolution maps of gibbon-human breaks of synteny (BOS), apply Hi-C in gibbon, measure an array of epigenetic features, and perform cross-species comparisons. We find that gibbon rearrangements occur at TAD boundaries, independent of the parameters used to identify TADs. This overlap is supported by a remarkable genetic and epigenetic similarity between BOS and TAD boundaries, namely presence of CpG islands and SINE elements, and enrichment in CTCF and H3K4me3 binding. Cross-species comparisons reveal that regions orthologous to BOS also correspond with boundaries of large (400-600kb) TADs in human and other mammalian species. The co-localization of rearrangement breakpoints and TAD boundaries may be due to higher chromatin fragility at these locations and/or increased selective pressure against rearrangements that disrupt TAD integrity. We also examine the small portion of BOS that did not overlap with TAD boundaries and gave rise to novel TADs in the gibbon genome. We postulate that these new TADs generally lack deleterious consequences. Lastly, we show that limited epigenetic homogenization occurs across breakpoints, irrespective of their time of occurrence in the gibbon lineage. Overall, our findings demonstrate remarkable conservation of chromatin interactions and epigenetic landscape in gibbons, in spite of extensive genomic shuffling.
2018-05-30 | GSE115062 | GEO
Project description:The relationship between evolutionary genome remodeling and the three-dimensional structure of the genome remain largely unexplored. Here we use the heavily rearranged gibbon genome to examine how evolutionary chromosomal rearrangements impact genome-wide chromatin interactions, topologically associating domains (TADs), and their epigenetic landscape. We use high-resolution maps of gibbon-human breaks of synteny (BOS), apply Hi-C in gibbon, measure an array of epigenetic features, and perform cross-species comparisons. We find that gibbon rearrangements occur at TAD boundaries, independent of the parameters used to identify TADs. This overlap is supported by a remarkable genetic and epigenetic similarity between BOS and TAD boundaries, namely presence of CpG islands and SINE elements, and enrichment in CTCF and H3K4me3 binding. Cross-species comparisons reveal that regions orthologous to BOS also correspond with boundaries of large (400-600kb) TADs in human and other mammalian species. The co-localization of rearrangement breakpoints and TAD boundaries may be due to higher chromatin fragility at these locations and/or increased selective pressure against rearrangements that disrupt TAD integrity. We also examine the small portion of BOS that did not overlap with TAD boundaries and gave rise to novel TADs in the gibbon genome. We postulate that these new TADs generally lack deleterious consequences. Lastly, we show that limited epigenetic homogenization occurs across breakpoints, irrespective of their time of occurrence in the gibbon lineage. Overall, our findings demonstrate remarkable conservation of chromatin interactions and epigenetic landscape in gibbons, in spite of extensive genomic shuffling.
2018-05-30 | GSE115064 | GEO
Project description:In this study, we observed the effects of different uterine leiomyoma driver mutations to tumor DNA methylation, chromatin activity and gene expression, to form a comprehensive view on the epigenetic consequences of the mutations.
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Project description:We previously found that a native lipoprotein mix with a high VLDL+LDL/HDL ratio causes a global de novoDNA methylation in THP-1 macrophages. In the present experiment we assessed the consequences of global lipoprotein-induced de novo DNA methylation on global gene expression in the same cells. Moreover, we sought to use gene expression array data to measure RNA expression levels for candidate factors mediating the epigenetic effects of lipoproteins. Keywords: comparison treated vs. control
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