ArticleThe EMBO journal2000
Sister chromatid gene conversion is a prominent double-strand break repair pathway in mammalian cells.
Article in The EMBO journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 283 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
283 citing papers in PubMed, 583 citations in OpenAlex.
- Trial
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- Pan-Cancer Genomic Scars of Alternative End Joining and Single-Strand Annealing.bioRxiv : the preprint server for biology · 2026Article
- Lesions initiating spontaneous mitotic crossover are minimally subject to non-homologous end joining.bioRxiv : the preprint server for biology · 2026Article
- Organization of replicated chromosomes by DNA loops and sister chromatid cohesion.Nature reviews. Molecular cell biology · 2026Review
- Haplotype-resolved reconstruction and functional interrogation of cancer karyotypes.Cell systems · 2026Article
- Break-induced replication is activated to repair R-loop-associated double-strand breaks in SETX-deficient cells.Cell reports · 2025Article
- Temporal control of human DNA replication licensing by CDK4/6-RB signalling and chemical genetics.Nature communications · 2025Article
- Genetic variation in recalcitrant repetitive regions of theGenome research · 2025Article
- Review
- Two-ended recombination at a Flp-nickase-broken replication fork.Molecular cell · 2025Article
- Mechanisms of tandem duplication in the cancer genome.DNA repair · 2025Review
- Homologous recombination promotes non-immunogenic mitotic cell death upon DNA damage.Nature cell biology · 2025Article
- Contraception as chemoprevention of ovarian cancer in BRCA1 and BRCA2 women.Hormones (Athens, Greece) · 2024Review
- Cell-type-specific consequences of mosaic structural variants in hematopoietic stem and progenitor cells.Nature genetics · 2024Article
- The impact of developmental stage, tissue type, and sex on DNA double-strand break repair in Drosophila melanogaster.PLoS genetics · 2024Article
- Developmental progression of DNA double-strand break repair deciphered by a single-allele resolution mutation classifier.Nature communications · 2024Article
- MutSβ protects common fragile sites by facilitating homology-directed repair at DNA double-strand breaks with secondary structures.Nucleic acids research · 2024Article
- Natural Biopolymer-Based Delivery of CRISPR/Cas9 for Cancer Treatment.Pharmaceutics · 2023Review
- Revolutionizing DNA repair research and cancer therapy with CRISPR-Cas screens.Nature reviews. Molecular cell biology · 2023Review
223 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
In mammalian cells, repair of DNA double-strand breaks (DSBs) occurs by both homologous and non-homologous mechanisms. By definition, homologous recombination requires a template with sufficient sequence identity to the damaged molecule in order to direct repair. We now show that the sister chromatid acts as a repair template in a substantial proportion of DSB repair events. The outcome of sister chromatid repair is primarily gene conversion unassociated with reciprocal exchange. This contrasts with expectations from the classical DSB repair model originally proposed for yeast meiotic recombination, but is consistent with models in which recombination is coupled intimately with replication. These results may explain why cytologically observable sister chromatid exchanges are induced only weakly by DNA-damaging agents that cause strand breaks, since most homologous repair events would not be observed. A preference for non-crossover events between sister chromatids suggests that crossovers, although genetically silent, may be disfavored for other reasons. Possibly, a general bias against crossing over in mitotic cells exists to reduce the potential for genome alterations when other homologous repair templates are utilized.
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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.