ArticleNature2013
Two replication fork maintenance pathways fuse inverted repeats to rearrange chromosomes.
Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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.
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.
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Who cites it
34 citing papers in PubMed, 43 citations in OpenAlex.
- RAD51 separation of function mutation disables replication fork maintenance but preserves DSB repair.iScience · 2024Article
- Article
- SETD2 safeguards the genome against isochromosome formation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Exonucleases: Degrading DNA to Deal with Genome Damage, Cell Death, Inflammation and Cancer.Cells · 2022Review
- Article
- Trex2 responds to damaged replication forks in diverse ways.Molecular & cellular oncology · 2021Article
- TREX2 Exonuclease Causes Spontaneous Mutations and Stress-Induced Replication Fork Defects in Cells Expressing RAD51Cell reports · 2020Article
- Suppression of mosaic mutation by co-delivery of CRISPR associated protein 9 and three-prime repair exonuclease 2 into porcine zygotes via electroporation.The Journal of reproduction and development · 2020Article
- Histone deposition promotes recombination-dependent replication at arrested forks.PLoS genetics · 2019Article
- DNA methylation at an enhancer of the three prime repair exonuclease 2 gene (TREX2) is linked to gene expression and survival in laryngeal cancer.Clinical epigenetics · 2019Article
- Structural insights into the duplex DNA processing of TREX2.Nucleic acids research · 2018Article
- Homologous recombination defects and how they affect replication fork maintenance.AIMS genetics · 2018Review
- Review
- Review
- Ubc13: the Lys63 ubiquitin chain building machine.Oncotarget · 2016Review
- Do DNA Double-Strand Breaks Drive Aging?Molecular cell · 2016Review
- A mechanism for 1,4-Benzoquinone-induced genotoxicity.Oncotarget · 2016Article
- The PCNA-associated protein PARI negatively regulates homologous recombination via the inhibition of DNA repair synthesis.Nucleic acids research · 2016Article
- Human HLTF mediates postreplication repair by its HIRAN domain-dependent replication fork remodelling.Nucleic acids research · 2015Article
- Multifaceted role of TREX2 in the skin defense against UV-induced skin carcinogenesis.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Replication fork maintenance pathways preserve chromosomes, but their faulty application at nonallelic repeats could generate rearrangements causing cancer, genomic disorders and speciation. Potential causal mechanisms are homologous recombination and error-free postreplication repair (EF-PRR). Homologous recombination repairs damage-induced DNA double-strand breaks (DSBs) and single-ended DSBs within replication. To facilitate homologous recombination, the recombinase RAD51 and mediator BRCA2 form a filament on the 3' DNA strand at a break to enable annealing to the complementary sister chromatid while the RecQ helicase, BLM (Bloom syndrome mutated) suppresses crossing over to prevent recombination. Homologous recombination also stabilizes and restarts replication forks without a DSB. EF-PRR bypasses DNA incongruities that impede replication by ubiquitinating PCNA (proliferating cell nuclear antigen) using the RAD6-RAD18 and UBC13-MMS2-RAD5 ubiquitin ligase complexes. Some components are common to both homologous recombination and EF-PRR such as RAD51 and RAD18. Here we delineate two pathways that spontaneously fuse inverted repeats to generate unstable chromosomal rearrangements in wild-type mouse embryonic stem (ES) cells. Gamma-radiation induced a BLM-regulated pathway that selectively fused identical, but not mismatched, repeats. By contrast, ultraviolet light induced a RAD18-dependent pathway that efficiently fused mismatched repeats. Furthermore, TREX2 (a 3'→5' exonuclease) suppressed identical repeat fusion but enhanced mismatched repeat fusion, clearly separating these pathways. TREX2 associated with UBC13 and enhanced PCNA ubiquitination in response to ultraviolet light, consistent with it being a novel member of EF-PRR. RAD18 and TREX2 also suppressed replication fork stalling in response to nucleotide depletion. Interestingly, replication fork stalling induced fusion for identical and mismatched repeats, implicating faulty replication as a causal mechanism for both pathways.
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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.