ArticleMolecular and cellular biology2003
Extensive loss of heterozygosity is suppressed during homologous repair of chromosomal breaks.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 119 citations in OpenAlex.
- The dynamics of RAD51 foci formation and elongation in living human cells.Nucleic acids research · 2026Article
- Megabase-scale loss of heterozygosity provoked by CRISPR-Cas9 DNA double-strand breaks.Molecular cell · 2025Article
- Technological and computational approaches to detect somatic mosaicism in epilepsy.Neurobiology of disease · 2023Review
- A spatial genome aligner for resolving chromatin architectures from multiplexed DNA FISH.Nature biotechnology · 2023Article
- Active genetics comes alive: Exploring the broad applications of CRISPR-based selfish genetic elements (or gene-drives): Exploring the broad applications of CRISPR-based selfish genetic elements (or gene-drives).BioEssays : news and reviews in molecular, cellular and developmental biology · 2022Review
- Mitotic Antipairing of Homologous Chromosomes.Results and problems in cell differentiation · 2022Article
- Distinct pathways of homologous recombination controlled by the SWS1-SWSAP1-SPIDR complex.Nature communications · 2021Article
- Article
- Chromothripsis as an on-target consequence of CRISPR-Cas9 genome editing.Nature genetics · 2021Article
- Homologous Recombination Subpathways: A Tangle to Resolve.Frontiers in genetics · 2021Review
- POLQ suppresses interhomolog recombination and loss of heterozygosity at targeted DNA breaks.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Single crossover-mediated targeted nucleotide substitution and knock-in strategies with CRISPR/Cas9 system in the rice blast fungus.Scientific reports · 2019Article
- Chromatin organization modulates the origin of heritable structural variations in human genome.Nucleic acids research · 2019Article
- The Post-Synaptic Function of Brca2.Scientific reports · 2019Article
- DNA Double Strand Breaks and Chromosomal Translocations Induced by DNA Topoisomerase II.Frontiers in molecular biosciences · 2019Review
- Inter-homologue repair in fertilized human eggs?Nature · 2018Article
- Homologous recombination occurs frequently at innate GT microsatellites in normal somatic and germ cells in vivo.BMC genomics · 2018Article
- Putting together and taking apart: assembly and disassembly of the Rad51 nucleoprotein filament in DNA repair and genome stability.Cell stress · 2018Review
- Induction of Chromosomal Translocations with CRISPR-Cas9 and Other Nucleases: Understanding the Repair Mechanisms That Give Rise to Translocations.Advances in experimental medicine and biology · 2018Review
- Genome-wide mapping of sister chromatid exchange events in single yeast cells using Strand-seq.eLife · 2017Article
5 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of heterozygosity (LOH) is a common genetic alteration in tumors and often extends several megabases to encompass multiple genetic loci or even whole chromosome arms. Based on marker and karyotype analysis of tumor samples, a significant fraction of LOH events appears to arise from mitotic recombination between homologous chromosomes, reminiscent of recombination during meiosis. As DNA double-strand breaks (DSBs) initiate meiotic recombination, a potential mechanism leading to LOH in mitotically dividing cells is DSB repair involving homologous chromosomes. We therefore sought to characterize the extent of LOH arising from DSB-induced recombination between homologous chromosomes in mammalian cells. To this end, a recombination reporter was introduced into a mouse embryonic stem cell line that has nonisogenic maternal and paternal chromosomes, as is the case in human populations, and then a DSB was introduced into one of the chromosomes. Recombinants involving alleles on homologous chromosomes were readily obtained at a frequency of 4.6 x 10(-5); however, this frequency was substantially lower than that of DSB repair by nonhomologous end joining or the inferred frequency of homologous repair involving sister chromatids. Strikingly, the majority of recombinants had LOH restricted to the site of the DSB, with a minor class of recombinants having LOH that extended to markers 6 kb from the DSB. Furthermore, we found no evidence of LOH extending to markers 1 centimorgan or more from the DSB. In addition, crossing over, which can lead to LOH of a whole chromosome arm, was not observed, implying that there are key differences between mitotic and meiotic recombination mechanisms. These results indicate that extensive LOH is normally suppressed during DSB-induced allelic recombination in dividing mammalian cells.
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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.