(Some) cellular mechanisms influencing the transcription of human endogenous retrovirus, HERV-Fc1

Magdalena Janina Laska, Kari Konstantin Nissen, Bjørn Andersen Nexø

Research output: Contribution to journalJournal articleResearchpeer-review


DNA methylation and histone acetylation are epigenetic modifications that act as regulators of gene expression. DNA methylation is considered an important mechanism for silencing of retroelements in the mammalian genome. However, the methylation of human endogenous retroviruses (HERVs) is not well investigated. The aim of this study was to investigate the transcriptional potential of HERV-Fc1 proviral 5'LTR in more detail, and examined the specific influence of CpG methylation on this LTR in number of cell lines. Specifically, the role of demethylating chemicals e.g. 5-aza-2' deoxycytidine and Trichostatin-A, in inducing or reactivating expression of HERV-Fc1 specific sequences and the mechanisms were investigated. In our present study, 5-aza-dC is shown to be a powerful inducer of HERV-Fc1, and at the same time it strongly inhibits methylation of DNA. Treatment with this demethylating agent 5-aza-dC, results in significantly increased levels of HERV-Fc1 expression in cells previously not expressing HERV-Fc1, or with a very low expression level. The extent of expression of HERV-Fc1 RNAs precisely correlates with the apparent extent of demethylation of the related DNA sequences. In conclusion, the results suggest that inhibition of DNA methylation/histone deacetylase can interfere with gene silencing mechanisms affecting HERV-Fc1 expression in human cells.

Original languageEnglish
JournalP L o S One
Issue number1
Pages (from-to)e53895
Publication statusPublished - 2013
Externally publishedYes


  • CpG Islands
  • DNA Methylation
  • azacitidine
  • cell Line, Tumor
  • endogenous Retroviruses
  • epigenesis, Genetic
  • gene Expression Regulation
  • humans
  • hydroxamic Acids
  • journal Article
  • promoter Regions, Genetic
  • research Support, Non-U.S. Gov't
  • retroelements
  • terminal Repeat Sequences
  • transcription, Genetic

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