ArticleGenome research2016
Sister chromatid telomere fusions, but not NHEJ-mediated inter-chromosomal telomere fusions, occur independently of DNA ligases 3 and 4.
Article in Genome research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Telomere-driven replicative crisis is driven by large-scale changes in genomic architecture.Genome research · 2026Article
- Mitotic microhomology-mediated break-induced replication promotes chromoanasynthesis.Nature communications · 2026Article
- Telomeres as hotspots for innate immunity and inflammation.DNA repair · 2024Review
- Double-strand breaks induce inverted duplication chromosome rearrangements by a DNA polymerase δ-dependent mechanism.Nature communications · 2023Article
- ATRX modulates the escape from a telomere crisis.PLoS genetics · 2022Article
- Article
- Target residence of Cas9-sgRNA influences DNA double-strand break repair pathway choices in CRISPR/Cas9 genome editing.Genome biology · 2022Article
- Mechanistic origins of diverse genome rearrangements in cancer.Seminars in cell & developmental biology · 2022Review
- Cell senescence and malignant transformation in the inherited bone marrow failure syndromes: Overlapping pathophysiology with therapeutic implications.Seminars in hematology · 2022Review
- Homologous recombination-mediated irreversible genome damage underlies telomere-induced senescence.Nucleic acids research · 2021Article
- UPF1 promotes the formation of R loops to stimulate DNA double-strand break repair.Nature communications · 2021Article
- Effect of DNA repair inhibitor AsiDNA on the incidence of telomere fusion in crisis.Human molecular genetics · 2021Article
- Structural variant evolution after telomere crisis.Nature communications · 2021Article
- Tracking telomere fusions through crisis reveals conflict between DNA transcription and the DNA damage response.NAR cancer · 2021Article
- Chromosome instability induced by a single defined sister chromatid fusion.Life science alliance · 2020Article
- Assembly and annotation of an Ashkenazi human reference genome.Genome biology · 2020Article
- Telomere fusions and translocations: a bridge too far?Current opinion in genetics & development · 2020Review
- Chromothripsis and telomere crisis: engines of genome instability.Current opinion in genetics & development · 2020Review
- Absence of XRCC4 and its paralogs in human cells reveal differences in outcomes for DNA repair and V(D)J recombination.DNA repair · 2020Article
- CtIP is essential for telomere replication.Nucleic acids research · 2019Article
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7 authors.
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Abstract
Telomeres shorten with each cell division and can ultimately become substrates for nonhomologous end-joining repair, leading to large-scale genomic rearrangements of the kind frequently observed in human cancers. We have characterized more than 1400 telomere fusion events at the single-molecule level, using a combination of high-throughput sequence analysis together with experimentally induced telomeric double-stranded DNA breaks. We show that a single chromosomal dysfunctional telomere can fuse with diverse nontelomeric genomic loci, even in the presence of an otherwise stable genome, and that fusion predominates in coding regions. Fusion frequency was markedly increased in the absence of TP53 checkpoint control and significantly modulated by the cellular capacity for classical, versus alternative, nonhomologous end joining (NHEJ). We observed a striking reduction in inter-chromosomal fusion events in cells lacking DNA ligase 4, in contrast to a remarkably consistent profile of intra-chromosomal fusion in the context of multiple genetic knockouts, including DNA ligase 3 and 4 double-knockouts. We reveal distinct mutational signatures associated with classical NHEJ-mediated inter-chromosomal, as opposed to alternative NHEJ-mediated intra-chromosomal, telomere fusions and evidence for an unanticipated sufficiency of DNA ligase 1 for these intra-chromosomal events. Our findings have implications for mechanisms driving cancer genome evolution.
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