ArticleNature genetics2025
Enhancer adoption by an LTR retrotransposon generates viral-like particles, causing developmental limb phenotypes.
Article in Nature genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- A Natural LTR Retrotransposon Insertion in the Promoter of GhNAC140-Dt Boosts Cotton Lint Yield.Plant biotechnology journal · 2026Article
- Viviparity and beyond: captured endogenous retroviral envelope genes drive teleost physiological innovations.Molecular biology and evolution · 2026Article
- Molecular effects of transposable element sequences in mammalian cells.Genome biology · 2025Review
- Article
- A retrotransposon caught red-handed in a curious case of missing digits.Nature genetics · 2025Article
- An endogenous retroviral element co-opts an upstream regulatory sequence to achieve somatic expression and mobility.Nucleic acids research · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Transposable elements (TEs) are scattered across mammalian genomes. Silencing of TEs prevents harmful effects caused by either global activation leading to genome instability or insertional mutations disturbing gene transcription. However, whether the activation of a TE can cause disease without directly affecting gene expression is largely unknown. Here we show that a TE insertion can adopt nearby regulatory activity, resulting in the production of cell-type-specific viral-like particles (VLPs) that affect embryo formation. Failure to silence an LTR retrotransposon inserted upstream of the Fgf8 gene results in their co-expression during mouse development. VLP assembly in the Fgf8-expressing cells of the developing limb triggers apoptotic cell death, resulting in a limb malformation resembling human ectrodactyly. The phenotype can be rescued by mutating the retrotransposon coding sequence, thus preventing its full endogenous retroviral cycle. Our findings illustrate that TE insertions can be incorporated into the local genomic regulatory landscape and that VLP production in post-implantation embryos can cause developmental defects.
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Registered trials
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