Literature DB >> 26627183

DNA methylation and transcription in HERV (K, W, E) and LINE sequences remain unchanged upon foreign DNA insertions.

Stefanie Weber1, Susan Jung2, Walter Doerfler1,3.   

Abstract

AIM: DNA methylation and transcriptional profiles were determined in the regulatory sequences of the human endogenous retroviral (HERV-K, -W, -E) and LINE-1.2 elements and were compared between non-transgenomic and plasmid-transgenomic cells.
METHODS: DNA methylation profiles in the HERV (K, W, E) and LINE sequences were determined by bisulfite genomic sequencing. The transcription of these genome segments was assessed by quantitative real-time PCR.
RESULTS: In HERV-K, HERV-W and LINE-1.2 the levels of DNA methylation ranged between 75 and 98%, while in HERV-E they were around 60%. Nevertheless, the HERV and LINE-1.2 sequences were actively transcribed. No differences were found in comparisons of HERV and LINE-1.2 CpG methylation and transcription patterns between non-transgenomic and plasmid-transgenomic HCT116 cells.
CONCLUSION: The insertion of a 5.6 kbp plasmid into the HCT116 genome had no effect on the HERV and LINE-1.2 methylation and transcription profiles, although other parts of the HCT116 genome had shown marked changes. These repetitive sequences are transcribed, probably because the large number of HERV and LINE-1.2 elements harbor copies with non- or hypo-methylated long terminal repeat sequences.

Entities:  

Keywords:  CpG methylation in HERV and LINE-1.2 DNA; bisulfite genomic sequencing; comparisons of methylation and transcription between non-transgenomic and transgenomic cells; human cell line HCT116; human endogenous retroviral (HERV-K,-W,-E) and LINE-1.2 sequences; plasmid-transgenomic HCT116 cells; quantitative real-time PCR

Mesh:

Year:  2015        PMID: 26627183     DOI: 10.2217/epi.15.109

Source DB:  PubMed          Journal:  Epigenomics        ISSN: 1750-192X            Impact factor:   4.778


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Review 3.  The Relationship of the Mechanisms of the Pathogenesis of Multiple Sclerosis and the Expression of Endogenous Retroviruses.

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