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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide hydroxymethylcytosine pattern changes in response to oxidative stress

ABSTRACT: The TET-family enzymes (TETs) convert methylcytosine to hydroxymethylcytosine, a lately discovered epigenetic modification that can modulate transcription. While recent reports suggest that TETs may play a role in response to oxidative stress, this role remains uncertain. Here we show that Tet1 is sensitive to peroxide and report a global decrease in hydroxymethylcytosine in cells treated with BSO and in the intestinal epithelium of mice lacking the major antioxidant enzymes glutathione peroxidases 1 and 2. Furthermore, genome-wide profiling revealed differentially hydroxymethylated regions in genes involved in responses to oxidative stress. Intriguingly, a considerable proportion of these regions lie in genes encoding microRNAs predicted to target transcripts involved in oxidative stress response. This work thus demonstrates a profound effect of oxidative stress on the hydroxymethylome and opens exciting new avenues of research by highlighting a set of microRNAs that may participate in the prevention or etiology of oxidative-stress-related diseases. Examination of DNA hydroxymethylation landscape in SY5Y cell lines and in intestinal epithelium of mice.

ORGANISM(S): Homo sapiens

SUBMITTER: Matthieu Defrance

PROVIDER: E-GEOD-59718 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide hydroxymethylcytosine pattern changes in response to oxidative stress

Project description:The TET-family enzymes (TETs) convert methylcytosine to hydroxymethylcytosine, a lately discovered epigenetic modification that can modulate transcription. While recent reports suggest that TETs may play a role in response to oxidative stress, this role remains uncertain. Here we show that Tet1 is sensitive to peroxide and report a global decrease in hydroxymethylcytosine in cells treated with BSO and in the intestinal epithelium of mice lacking the major antioxidant enzymes glutathione peroxidases 1 and 2. Furthermore, genome-wide profiling revealed differentially hydroxymethylated regions in genes involved in responses to oxidative stress. Intriguingly, a considerable proportion of these regions lie in genes encoding microRNAs predicted to target transcripts involved in oxidative stress response. This work thus demonstrates a profound effect of oxidative stress on the hydroxymethylome and opens exciting new avenues of research by highlighting a set of microRNAs that may participate in the prevention or etiology of oxidative-stress-related diseases.

2016-01-14 | GSE59718 | GEO

Expression data from intestinal epithelium

Project description:Oxidative stress and celllular apoptosis of intestinal epithelial tissues relies on the environments from drinking different waters. In the rat intestinal epithelium, the toxic materials or antioxidant materials may affect the genes expression of oxidative stress and apoptosis through the oral intake ofa waters or agents. The up- or down-regulation in the antioxidant genes and apoptosis-related genes may represent the internal microenvironments in the intestine. Therefore, we used intestinal epithelium from rats drinking different waters to test the several genes expression. We used microarrays to detail the global programme of gene expression underlying damage or protection effect and identified distinct classes of up-regulated or down-regulated genes during drinking different waters test in this process.

2014-12-01 | GSE55142 | GEO

Autophagy maintains intestinal stem cell integrity

Project description:The intestinal epithelium is continuously renewed by a pool of intestinal stem cells expressing Lgr5. We show that deletion of the key autophagy gene Atg7 affects the survival of Lgr5+ intestinal stem cells. Mechanistically, this involves defective DNA repair, oxidative stress, and altered interactions with the microbiota. This study highlights the importance of autophagy in maintaining the integrity of intestinal stem cells.

2020-05-28 | GSE136952 | GEO

5-hydroxymethylcytosine and gene activity in mouse intestinal differentiation (RNA-Seq).

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

5-hydroxymethylcytosine and gene activity in mouse intestinal differentiation (hmeDIP-seq).

2019-06-13 | GSE132631 | GEO

Intestinal stem cell differentiation is associated with dynamic changes in the chromatin landscape [5hmc-seal-seq]

Project description:The global localization of 5-hydroxymethylcytosine (5hmc) were measured by 5hmc-seal-seq in four populations of intestinal epithelium defined by their levels of a GFP reporter transgene that is driven by the regulatory elements of the Sox9 gene.

2019-05-24 | GSE131245 | GEO

TET-dependent regulation of retrotransposable elements in mouse embryonic stem cells [small RNA-seq]

Project description:TET enzymes oxidise DNA methylation as part of an active demethylation pathway. Despite extensive research into the role of TETs in genome regulation, little is known about their effect on transposable elements (TEs), which make up nearly half of the mouse and human genomes. Epigenetic mechanisms controlling TEs have the potential to affect their mobility and to drive the co-adoption of TEs for the benefit of the host. We have performed a detailed investigation of the role of TET enzymes in the regulation of TEs in mouse embryonic stem cells (ESCs). We found that TET1 and TET2 bind multiple TE classes that harbour a variety of epigenetic signatures indicative of different functional roles. Namely, TETs co-bind with pluripotency factors to enhancer-like TEs that interact with highly expressed genes in ESCs, whose expression is partly maintained by the demethylating action of TET2. TETs and 5-hydroxymethylcytosine are also strongly enriched at the 5’ UTR of full-length, evolutionarily young LINE1 elements, a pattern that is conserved in human embryonic stem cells. TET depletion leads to a marked increase in DNA methylation levels at LINE1s, but surprisingly their expression is stably maintained through additional TET-dependent activities. Specifically, we find that TET1 recruits the SIN3A co-repressive complex to LINE1s, ensuring their repression upon TET-driven hypomethylation. This dual nature of TET action may reflect the evolutionary battle between TEs and the host. Our data implicate TET enzymes in the evolutionary dynamics of TEs, both in the context of exaptation processes and of retrotransposition control.

2016-10-28 | GSE84459 | GEO

TET-dependent regulation of retrotransposable elements in mouse embryonic stem cells [RNA-seq]

2016-10-28 | GSE84458 | GEO

Genome-wide hydroxymethylcytosine pattern changes in response to oxidative stress

Project description:Genome-wide hydroxymethylcytosine pattern changes in response to oxidative stress

| PRJNA256032 | ENA

ATAC-sequencing mice small intestinal epithelium with intestinal epithelium specific LSD1 knock out compared to wild type

Project description:To study the epigenetic regulation of intestinal epithelium we focus on the role of chromatin modulators. Lysine-specific histone demethylase 1a (KDM1A, LSD1) is one of the enzymes that can erase the H3K4me1/2 mark. To assess the role of LSD1 in intestinal epithelium we studied wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (KO) (Villin-Cre+; Lsd1f/f) mice. We found that KO mice completely lack Paneth cells, and have altered stem cell characteristics compared to WT littermates. To assess genome-wide ATAC levels in WT and KO small intestines, we isolated intestinal epithelium tissue from wild type mice and LSD1 KO mice. This tissue was digested to single cells and performed ATAC seq as described in the protocols.

2021-03-23 | E-MTAB-8718 | biostudies-arrayexpress

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