5-hydroxymethylcytosine and gene activity in mouse intestinal differentiation (hmeDIP-seq).
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ABSTRACT:
PROVIDER: PRJNA548546 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9285870.fastq.gz | Fastqsanger.gz | |||
| SRR9285871.fastq.gz | Fastqsanger.gz | |||
| SRR9285862.fastq.gz | Fastqsanger.gz | |||
| SRR9285872.fastq.gz | Fastqsanger.gz | |||
| SRR9285863.fastq.gz | Fastqsanger.gz |
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Project description:Background: Cytosine hydroxymethylation (5hmC) was recently identified in mammalian DNA as the product of oxidation of methylated cytosines (5mC) by Ten-Eleven-Translocation (TET) enzymes. The TETs have been shown to influence 5mC metabolism, pluripotency and differentiation during early embryonic development. However, a functional relationship between gene expression and 5hmC in adult (somatic) stem cell differentiation is however mainly unknown. To explore the role of this novel DNA modification in adult stem cell differentiation we profiled 5hmC and gene activity in purified mouse intestinal progenitors and differentiated progeny. Results: We show that the hydroxymethylome is highly dynamic with tens of thousands of differentially hydroxymethylated regions between progenitors and differentiated progeny. In progenitors 5hmC does not correlate with gene expression levels, however, upon differentiation a global increase in 5hmC is observed with an overall positive correlation between 5hmC and gene expression together with prominent associations with histone modifications that typify active genes and enhancer elements. Conclusions: In the context of recent evidence of near identical methylomes between mouse intestinal stem and differentiated cells, our data imply that a gene regulatory role for 5hmC is predominant over its role in controlling DNA methylation states. Our study provides an insight into the dynamics of 5hmC and of epigenetic machineries in differentiation of the mouse intestine.
2019-06-13 | GSE132631 | GEO
Project description:We investigated genome-wide analysis of 5-hydroxymethylcytosine (5hmC) distribution in mouse intestinal stem and differentiated cells using hydroxyMethylated DNA immunoprecipitation (hMeDIP) followed by sequencing. Genomic DNA from mouse intestinal stem (Lgr5+) and villus differentiated cells were sonicated, immunoprecipitated by a 5hmC antibody, and sequenced in order to identify differential hydroxymethylated regions and genes.
2016-11-23 | E-MTAB-5202 | biostudies-arrayexpress
Project description:5-hydroxymethylcytosine and gene activity in mouse intestinal differentiation (RNA-Seq).
| PRJNA548554 | ENA
Project description:Background: Cytosine hydroxymethylation (5hmC) was recently identified in mammalian DNA as the product of oxidation of methylated cytosines (5mC) by Ten-Eleven-Translocation (TET) enzymes. The TETs have been shown to influence 5mC metabolism, pluripotency and differentiation during early embryonic development. However, a functional relationship between gene expression and 5hmC in adult (somatic) stem cell differentiation is however mainly unknown. To explore the role of this novel DNA modification in adult stem cell differentiation we profiled 5hmC and gene activity in purified mouse intestinal progenitors and differentiated progeny. Results: We show that the hydroxymethylome is highly dynamic with tens of thousands of differentially hydroxymethylated regions between progenitors and differentiated progeny. In progenitors 5hmC does not correlate with gene expression levels, however, upon differentiation a global increase in 5hmC is observed with an overall positive correlation between 5hmC and gene expression together with prominent associations with histone modifications that typify active genes and enhancer elements. Conclusions: In the context of recent evidence of near identical methylomes between mouse intestinal stem and differentiated cells, our data imply that a gene regulatory role for 5hmC is predominant over its role in controlling DNA methylation states. Our study provides an insight into the dynamics of 5hmC and of epigenetic machineries in differentiation of the mouse intestine.
2019-06-13 | GSE132632 | GEO
Project description:Differentiation of CD4+T-cells into effector subsets is a critical component of the adaptive immune system and an incorrect response can lead to autoimmunity or immune deficiency. Cellular differentiation including T-cell differentiation is accompanied by large-scale epigenetic remodeling, including changes in DNA methylation at key regulators of T-cell differentiation. The TET family of enzymes were recently shown to be able to catalyse methylated cytosine (5mC) into 5-hydroxymethylcytosine (5hmC) enabling a pathway of active removal of DNA methylation. Here, we characterize 5hmC, 5mC and transcriptional dynamics during human CD4+T-cell polarisation in a time series approach and relate these changes to profiles in ex-vivo CD4+memory subsets. We observed large-scale remodelling during early CD4+T-cell differentiation which was predictive of subsequent changes during late time points, these changes were also related to disease associated regions which we show can act as functional regulatory elements. This dataset was designed to assess how 5-hydroxymethylcytosine (5hmC) changes over time during human CD4+T-cell polarization towards Th1 and Th2. We tested an early (1 day) and late (5 day) timepoint to distinguish between replication-independent (early) and replication-dependent (late) changes. When comparing the time-series profiles, we observed an early gain followed by a late loss of 5hmC suggesting active 5hmC remodelling precedes lineage specification in CD4+T-cells. This submission contains the data from genome-wide 5-hydroxymethylcytosine (5hmC) profiling by hMeDIP-seq in primary human CD4+T-cells polarized towards Th1 and Th2 time-series. This submission is part of series containing 5hmC and DNA methylation profiling of the same samples. See related experiments E-MTAB-4685, E-MTAB-4687, E-MTAB-4688, E-MTAB-4689.
2016-07-11 | E-MTAB-4686 | biostudies-arrayexpress
Project description:DNA methylation and hydroxymethylation have been implicated in normal development and differentiation, but our knowledge about the genome-wide distribution of 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) during cellular differentiation remains limited. Using in vitro model system of gradual differentiation of human embryonic stem (hES) cells into ventral midbrain-type neural precursor (NP) cells and terminally into dopamine (DA) neurons, we explored changes in 5mC or 5hmC patterns during lineage commitment. We used three techniques, 450K DNA methylation array, MBD-seq, and hMeDIP-seq, and found combination of these methods can provide comprehensive information on the genome-wide 5mC or 5hmC patterns. We observed dramatic changes of 5mC patterns during differentiation of hES cells into NP cells. Although genome-wide 5hmC distribution was more stable than 5mC, coding exons, CpG islands and shores showed dynamic 5hmC patterns during differentiation. In addition to the role of DNA methylation as a mechanism to initiating gene silencing, we also found DNA methylation as a locking system to maintain gene silencing. More than 1,000 genes including mesoderm development related genes acquired promoter methylation during neuronal differentiation even though they were already silenced in hES cells. Finally, we found that activated genes lost 5mC in transcription start site (TSS) but acquired 5hmC around TSS and gene body during differentiation. Our findings may provide clues for elucidating the molecular mechanisms underlying lineage specific differentiation of pluripotent stem cells during human embryonic development. Examination of hMeDIP-Seq and MBD-Seq in 3 cell types (human embryonic stem, neural precursor, and dopamine neuron cells)
2013-11-04 | E-GEOD-38214 | biostudies-arrayexpress
Project description:Ten-eleven translocation (Tet) hydroxylases (Tet1-3) oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). In neurons increased 5hmC levels within gene bodies correlate positively with gene expression. Here, we studied 5hmC profiles (hMeDIP) during retinal maturation between postnatal week 2 and postnatal week 3 using HiSeq 2000 instrument.
2015-04-02 | GSE65860 | GEO
Project description:hMeDIP-seq of mouse intestinal stem and differentiated cells
| PRJEB18014 | ENA
Project description:Cytosine hydroxymethylation (5hmC) in mammalian DNA is the product of oxidation of methylated cytosines (5mC) by Ten-Eleven-Translocation (TET) enzymes. While it has been shown that the TETs influence 5mC metabolism, pluripotency and differentiation during early embryonic development, the functional relationship between gene expression and 5hmC in adult (somatic) stem cell differentiation is still unknown. Here we report that 5hmC levels undergo highly dynamic changes during adult stem cell differentiation from intestinal progenitors to differentiated intestinal epithelium. We profiled 5hmC and gene activity in purified mouse intestinal progenitors and differentiated progeny to identify 43425 differentially hydroxymethylated regions and 5325 differentially expressed genes. These differentially marked regions showed both losses and gains of 5hmC after differentiation, despite lower global levels of 5hmC in progenitor cells. In progenitors, 5hmC did not correlate with gene transcript levels, however, upon differentiation the global increase in 5hmC content showed an overall positive correlation with gene expression level as well as prominent associations with histone modifications that typify active genes and enhancer elements. Our data support a gene regulatory role for 5hmC that is predominant over its role in controlling DNA methylation states.
| S-EPMC6969059 | biostudies-literature
Project description:We profiled 5-hydroxymethylcytosine patterns in hippocampi using hydroxymethylated DNA immunoprecipitation followed by Illumina deep sequencing (hMeDIP-Seq). We profiled the hippocampi of 4 young (3 month old) and 4 aged (18 month old) C57BL/6 mice. Additionally, we profiled the 5-hmC patterns of hippocampi that were stereotactically injected with lentiviral constructs that overexpressed Tet2 or luciferase.
2018-02-25 | GSE102473 | GEO