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10:10
Retroviral Scanning: Mapping MLV Integration Sites to Define Cell-specific Regulatory Regions
Published on: May 28, 2017
Epigenetic interplay between mouse endogenous retroviruses and host genes
Genome Biology
|October 5, 2012
Summary
DNA methylation spreading from endogenous retroviruses (ERVs) to nearby genes is rare. Active genes can protect themselves from silencing by blocking repressive marks or spreading active chromatin toward ERVs.
Area of Science:
- Epigenetics
- Genomics
- Molecular Biology
Background:
- Transposable elements, including endogenous retroviruses (ERVs), are subject to epigenetic silencing via DNA methylation.
- The potential for DNA methylation to spread from ERVs to adjacent genes and induce silencing is a key area of investigation.
Purpose of the Study:
- To investigate the DNA methylation status of mouse ERVs near genes.
- To understand how ERV methylation influences nearby gene expression and vice versa.
Main Methods:
- Assessed DNA methylation states of ERVs (ETn/MusD and IAP families) in mouse tissues.
- Analyzed methylation patterns in relation to gene proximity and expression.
- Examined epigenetic marks (H3K4me3, CTCF) at ERV-gene boundaries.
Main Results:
- ETn/MusD ERVs showed decreased DNA methylation near expressed genes.
- IAP ERVs were generally heavily methylated, irrespective of genomic context.
- Differential methylation between LTRs of full-length ETn and IAP copies was observed.
- Spreading of DNA methylation from ERVs to genes was rare; boundaries enriched with H3K4me3 and CTCF were identified.
- Unmethylated ERV flanking regions showed H3K4me3, indicating euchromatin spread from genes.
Conclusions:
- Spreading of DNA methylation from ERVs to active gene promoters is infrequent.
- Genes are protected from ERV-induced silencing through mechanisms that block repressive marks or promote euchromatin spread toward ERVs.
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