Genome-wide hydroxymethylcytosine pattern changes in response to oxidative stress
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA256032 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1523750.fastq.gz | Fastqsanger.gz | |||
| SRR1523745.fastq.gz | Fastqsanger.gz | |||
| SRR1523746.fastq.gz | Fastqsanger.gz | |||
| SRR1523747.fastq.gz | Fastqsanger.gz | |||
| SRR1523748.fastq.gz | Fastqsanger.gz |
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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. Examination of DNA hydroxymethylation landscape in SY5Y cell lines and in intestinal epithelium of mice.
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