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Human TRIM5α senses and restricts LINE-1 elements.

Bianca Volkmann1, Sabine Wittmann1, Justine Lagisquet1

  • 1Institute of Clinical and Molecular Virology, Friedrich Alexander University Erlangen-Nürnberg, 91054 Erlangen, Germany.

Proceedings of the National Academy of Sciences of the United States of America
|July 12, 2020
PubMed
Summary

The intrinsic immune factor TRIM5α restricts and senses LINE-1 retroelements in human cells. This interaction activates innate immune signaling, protecting genomic integrity from mobile genetic elements.

Keywords:
LINE-1TRIM5αinnate immune sensingrestriction factorretrotransposon

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Area of Science:

  • Genetics
  • Molecular Biology
  • Immunology

Background:

  • Mobile genetic elements, particularly LINE-1 retroelements, are active in the human genome.
  • LINE-1 retrotransposition can cause detrimental genomic consequences.
  • Cells possess mechanisms to control LINE-1 activity to maintain genome stability.

Purpose of the Study:

  • To investigate the role of the intrinsic immune factor TRIM5α in controlling LINE-1 retroelements.
  • To determine if TRIM5α can sense and restrict human LINE-1 retrotransposition.
  • To elucidate the mechanisms by which TRIM5α interacts with and regulates LINE-1.

Main Methods:

  • Cell-based assays to assess LINE-1 retrotransposition.
  • Co-immunoprecipitation to study TRIM5α-LINE-1 interactions.
  • Analysis of innate immune signaling pathways (AP-1, NF-κB) activation.

Main Results:

  • Both human and rhesus TRIM5α efficiently repress human LINE-1 retrotransposition.
  • TRIM5α interacts with LINE-1 ribonucleoprotein complexes in the cytoplasm, which is crucial for restriction.
  • TRIM5α engagement with LINE-1 triggers innate immune signaling, activating AP-1 and NF-κB, leading to LINE-1 promoter down-regulation.

Conclusions:

  • TRIM5α acts as a pattern recognition receptor that restricts and senses LINE-1 retroelements.
  • TRIM5α employs distinct mechanisms to control LINE-1, safeguarding the human genome.
  • This study reveals a novel role for TRIM5α in defending against mobile genetic elements.