Interplay of TRIM28 and DNA methylation in controlling human endogenous retroelements

Genome Res. 2014 Aug;24(8):1260-70. doi: 10.1101/gr.172833.114. Epub 2014 May 30.

Abstract

Reverse transcription-derived sequences account for at least half of the human genome. Although these retroelements are formidable motors of evolution, they can occasionally cause disease, and accordingly are inactivated during early embryogenesis through epigenetic mechanisms. In the mouse, at least for endogenous retroviruses, important mediators of this process are the tetrapod-specific KRAB-containing zinc finger proteins (KRAB-ZFPs) and their cofactor TRIM28. The present study demonstrates that KRAB/TRIM28-mediated regulation is responsible for controlling a very broad range of human-specific endogenous retroelements (EREs) in human embryonic stem (ES) cells and that it exerts, as a consequence, a marked effect on the transcriptional dynamics of these cells. It further reveals reciprocal dependence between TRIM28 recruitment at specific families of EREs and DNA methylation. It finally points to the importance of persistent TRIM28-mediated control of ERE transcriptional impact beyond their presumed inactivation by DNA methylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alu Elements
  • Animals
  • Cell Line
  • DNA Methylation*
  • Embryonic Stem Cells
  • Endogenous Retroviruses / genetics
  • Gene Expression Regulation
  • Humans
  • Mice
  • Repressor Proteins / physiology*
  • Transcription, Genetic
  • Tripartite Motif-Containing Protein 28

Substances

  • Repressor Proteins
  • TRIM28 protein, human
  • Tripartite Motif-Containing Protein 28