ArticleMolecular and cellular biology1997
Chromosomal double-strand breaks induce gene conversion at high frequency in mammalian cells.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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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
92 citing papers in PubMed, 174 citations in OpenAlex.
- Break-induced replication is activated to repair R-loop-associated double-strand breaks in SETX-deficient cells.Cell reports · 2025Article
- Estimating Gene Conversion Tract Length and Rate From PacBio HiFi Data.Molecular biology and evolution · 2025Article
- Analyzing Homologous Recombination Using Antibiotic Marker Substrates in Mammalian Cells.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Transgenic mice harboring direct repeat substrates reveal key underlying causes of homologous recombination in vivo.DNA repair · 2022Review
- PIF1 helicase promotes break-induced replication in mammalian cells.The EMBO journal · 2021Article
- Centromeres under Pressure: Evolutionary Innovation in Conflict with Conserved Function.Genes · 2020Review
- High-throughput creation and functional profiling of DNA sequence variant libraries using CRISPR-Cas9 in yeast.Nature biotechnology · 2018Article
- Frequent nonallelic gene conversion on the human lineage and its effect on the divergence of gene duplicates.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- FANCJ helicase controls the balance between short- and long-tract gene conversions between sister chromatids.Nucleic acids research · 2017Article
- TALEN-Mediated FLAG-Tagging of Endogenous Histone Methyltransferase DOT1L.Advances in bioscience and biotechnology (Print) · 2017Article
- Complex Breakpoints and Template Switching Associated with Non-canonical Termination of Homologous Recombination in Mammalian Cells.PLoS genetics · 2016Article
- Efficient introduction of specific homozygous and heterozygous mutations using CRISPR/Cas9.Nature · 2016Article
- Gene editing toward the use of autologous therapies in recessive dystrophic epidermolysis bullosa.Translational research : the journal of laboratory and clinical medicine · 2016Review
- Novel Biological Approaches for Testing the Contributions of Single DSBs and DSB Clusters to the Biological Effects of High LET Radiation.Frontiers in oncology · 2016Review
- Towards a new era in medicine: therapeutic genome editing.Genome biology · 2015Review
- EEPD1 Rescues Stressed Replication Forks and Maintains Genome Stability by Promoting End Resection and Homologous Recombination Repair.PLoS genetics · 2015Article
- Deciphering the Code of the Cancer Genome: Mechanisms of Chromosome Rearrangement.Trends in cancer · 2015Article
- Massive interstitial copy-neutral loss-of-heterozygosity as evidence for cancer being a disease of the DNA-damage response.BMC medical genomics · 2015Article
- Transcription and recombination: when RNA meets DNA.Cold Spring Harbor perspectives in biology · 2014Review
- Rosa26-GFP direct repeat (RaDR-GFP) mice reveal tissue- and age-dependence of homologous recombination in mammals in vivo.PLoS genetics · 2014Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Double-strand breaks (DSBs) stimulate chromosomal and extrachromosomal recombination and gene targeting. Transcription also stimulates spontaneous recombination by an unknown mechanism. We used Saccharomyces cerevisiae I-SceI to stimulate recombination between neo direct repeats in Chinese hamster ovary (CHO) cell chromosomal DNA. One neo allele was controlled by the dexamethasone-inducible mouse mammary tumor virus promoter and inactivated by an insertion containing an I-SceI site at which DSBs were introduced in vivo. The other neo allele lacked a promoter but carried 12 phenotypically silent single-base mutations that create restriction sites (restriction fragment length polymorphisms). This system allowed us to generate detailed conversion tract spectra for recipient alleles transcribed at high or low levels. Transient in vivo expression of I-SceI increased homologous recombination 2,000- to 10,000-fold, yielding recombinants at frequencies as high as 1%. Strikingly, 97% of these products arose by gene conversion. Most products had short, bidirectional conversion tracts, and in all cases, donor neo alleles (i.e., those not suffering a DSB) remained unchanged, indicating that conversion was fully nonreciprocal. DSBs in exogenous DNA are usually repaired by end joining requiring little or no homology or by nonconservative homologous recombination (single-strand annealing). In contrast, we show that chromosomal DSBs are efficiently repaired via conservative homologous recombination, principally gene conversion without associated crossing over. For DSB-induced events, similar recombination frequencies and conversion tract spectra were found under conditions of low and high transcription. Thus, transcription does not further stimulate DSB-induced recombination, nor does it appear to affect the mechanism(s) by which DSBs induce gene conversion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.