ArticleMolecular and cellular biology2000
Coupled homologous and nonhomologous repair of a double-strand break preserves genomic integrity in mammalian cells.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
105 citing papers in PubMed.
- Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025Review
- A comparative analysis of planarian genomes reveals regulatory conservation in the face of rapid structural divergence.Nature communications · 2024Article
- Discovery of novel DNA-damaging agents through phenotypic screening for DNA double-strand break.Cancer science · 2023Article
- Review
- Optimized two-step electroporation process to achieve efficient nonviral-mediated gene insertion into primary T cells.FEBS open bio · 2022Article
- Evaluation of Epigenetic and Radiomodifying Effects during Radiotherapy Treatments in Zebrafish.International journal of molecular sciences · 2021Review
- Review
- CRISPR/Cas9-Mediated Multi-Allelic Gene Targeting in Sugarcane Confers Herbicide Tolerance.Frontiers in genome editing · 2021Article
- Strong suppression of gene conversion with increasing DNA double-strand break load delimited by 53BP1 and RAD52.Nucleic acids research · 2020Article
- Precise in vivo genome editing via single homology arm donor mediated intron-targeting gene integration for genetic disease correction.Cell research · 2019Article
- Development of microtiter plate scale CRISPR/Cas9 transformation method forFungal biology and biotechnology · 2019Article
- CCR5 Governs DNA Damage Repair and Breast Cancer Stem Cell Expansion.Cancer research · 2018Article
- Repair of a Site-Specific DNA Cleavage: Old-School Lessons for Cas9-Mediated Gene Editing.ACS chemical biology · 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
- Precision genome editing using synthesis-dependent repair of Cas9-induced DNA breaks.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- The homologous recombination protein RAD51D protects the genome from large deletions.Nucleic acids research · 2017Article
- Complex Breakpoints and Template Switching Associated with Non-canonical Termination of Homologous Recombination in Mammalian Cells.PLoS genetics · 2016Article
- The democratization of gene editing: Insights from site-specific cleavage and double-strand break repair.DNA repair · 2016Review
- Homologous recombination and human health: the roles of BRCA1, BRCA2, and associated proteins.Cold Spring Harbor perspectives in biology · 2015Review
45 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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA double-strand breaks (DSBs) may be caused by normal metabolic processes or exogenous DNA damaging agents and can promote chromosomal rearrangements, including translocations, deletions, or chromosome loss. In mammalian cells, both homologous recombination and nonhomologous end joining (NHEJ) are important DSB repair pathways for the maintenance of genomic stability. Using a mouse embryonic stem cell system, we previously demonstrated that a DSB in one chromosome can be repaired by recombination with a homologous sequence on a heterologous chromosome, without any evidence of genome rearrangements (C. Richardson, M. E. Moynahan, and M. Jasin, Genes Dev., 12:3831-3842, 1998). To determine if genomic integrity would be compromised if homology were constrained, we have now examined interchromosomal recombination between truncated but overlapping gene sequences. Despite these constraints, recombinants were readily recovered when a DSB was introduced into one of the sequences. The overwhelming majority of recombinants showed no evidence of chromosomal rearrangements. Instead, events were initiated by homologous invasion of one chromosome end and completed by NHEJ to the other chromosome end, which remained highly preserved throughout the process. Thus, genomic integrity was maintained by a coupling of homologous and nonhomologous repair pathways. Interestingly, the recombination frequency, although not the structure of the recombinant repair products, was sensitive to the relative orientation of the gene sequences on the interacting chromosomes.
Indexed as
Identifiers
What OpenQuestion holds
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.