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LTR-Retrotransposon Control by tRNA-Derived Small RNAs.

Cell | 2017

Transposon reactivation is an inherent danger in cells that lose epigenetic silencing during developmental reprogramming. In the mouse, long terminal repeat (LTR)-retrotransposons, or endogenous retroviruses (ERV), account for most novel insertions and are expressed in the absence of histone H3 lysine 9 trimethylation in preimplantation stem cells. We found abundant 18 nt tRNA-derived small RNA (tRF) in these cells and ubiquitously expressed 22 nt tRFs that include the 3' terminal CCA of mature tRNAs and target the tRNA primer binding site (PBS) essential for ERV reverse transcription. We show that the two most active ERV families, IAP and MusD/ETn, are major targets and are strongly inhibited by tRFs in retrotransposition assays. 22 nt tRFs post-transcriptionally silence coding-competent ERVs, while 18 nt tRFs specifically interfere with reverse transcription and retrotransposon mobility. The PBS offers a unique target to specifically inhibit LTR-retrotransposons, and tRF-targeting is a potentially highly conserved mechanism of small RNA-mediated transposon control.

Pubmed ID: 28666125 RIS Download

Associated grants

  • Agency: NIGMS NIH HHS, United States
    Id: R01 GM076396
  • Agency: NCI NIH HHS, United States
    Id: P30 CA045508
  • Agency: NIGMS NIH HHS, United States
    Id: R01 GM067014
  • Agency: NIH HHS, United States
    Id: S10 OD020122
  • Agency: Howard Hughes Medical Institute, United States

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This is a list of tools and resources that we have found mentioned in this publication.


SAM format (tool)

RRID:SCR_012093

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RRID:SCR_012954

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RRID:SCR_016368

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RRID:SCR_011841

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Bowtie (software resource)

RRID:SCR_005476

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