ArticleNature structural & molecular biology2023
Fanconi anemia DNA crosslink repair factors protect against LINE-1 retrotransposition during mouse development.
Article in Nature structural & molecular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Active Human Transposable Elements: Long-Read Sequencing Technologies, Computational Analysis, and Implications for Human Disease.Biomolecules · 2026Review
- Functional analyses identify the L1 ORF2p Cryptic domain as a hub for intramolecular interfaces required for retrotransposition.Nucleic acids research · 2026Article
- Dynamic and Ongoing De Novo L1 Retrotransposition Contributes to Genome Plasticity and Intrapatient Heterogeneity in Ovarian Cancer.Cancer research · 2026Article
- Fancl-mutant mice reveal central role of monoubiquitination in Fanconi anemia and a model for therapeutic gene editing.Blood advances · 2026Article
- The Fanconi anemia pathway repairs colibactin-induced DNA interstrand cross-links.Nature communications · 2025Article
- Loss of Fanconi anemia proteins causes a reliance on lysosomal exocytosis.Cell death & disease · 2025Article
- Antagonistic regulation of LINE-1/Alu elements and their repressor APOBEC3B in cellular senescence.Mobile DNA · 2025Article
- Transposable elements in health and disease: Molecular basis and clinical implications.Chinese medical journal · 2025Review
- HELQ Maintains Genome Stability of Primordial Germ Cells by Inhibiting LINE-1 Expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Ultrarare Variants in DNA Damage Repair Genes in Pediatric Acute-Onset Neuropsychiatric Syndrome or Acute Behavioral Regression in Neurodevelopmental Disorders.Developmental neuroscience · 2025Article
- Chromosomal rearrangements and instability caused by the LINE-1 retrotransposon.bioRxiv : the preprint server for biology · 2024Article
- A minimal Fanconi Anemia complex in early diverging fungi.Scientific reports · 2024Article
- LINE-1 retrotransposition and its deregulation in cancers: implications for therapeutic opportunities.Genes & development · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Long interspersed nuclear element 1 (LINE-1) is the only autonomous retrotransposon in humans and new integrations are a major source of genetic variation between individuals. These events can also lead to de novo germline mutations, giving rise to heritable genetic diseases. Recently, a role for DNA repair in regulating these events has been identified. Here we find that Fanconi anemia (FA) DNA crosslink repair factors act in a common pathway to prevent retrotransposition. We purify recombinant SLX4-XPF-ERCC1, the crosslink repair incision complex, and find that it cleaves putative nucleic acid intermediates of retrotransposition. Mice deficient in upstream crosslink repair signaling (FANCA), a downstream component (FANCD2) or the nuclease XPF-ERCC1 show increased LINE-1 retrotransposition in vivo. Organisms limit retrotransposition through transcriptional silencing but this protection is attenuated during early development leaving the zygote vulnerable. We find that during this window of vulnerability, DNA crosslink repair acts as a failsafe to prevent retrotransposition. Together, our results indicate that the FA DNA crosslink repair pathway acts together to protect against mutation by restricting LINE-1 retrotransposition.
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