ArticleNucleic acids research2019
Repair of base damage within break-induced replication intermediates promotes kataegis associated with chromosome rearrangements.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 46 citations in OpenAlex.
- Break-induced replication forms long mutable single-strand DNA during meiosis.Nature communications · 2026Article
- Single base focal hypermutation cooccurs with structural variation as an early event in advanced prostate tumourigenesis with ancestry specific independence: a multi-ancestral observational study.Genome medicine · 2026Observational
- Genomic Instability and Adaptive Evolution Induced by RFA Insufficiency inCurrent issues in molecular biology · 2026Article
- Genome-wide screen reveals dependence of break induced replication on several distinct checkpoints.Nature communications · 2025Article
- Single base focal hypermutation cooccurs with structural variation as an early event in advanced prostate tumourigenesis with ancestry specific independence: a multi-ancestral observational study.Research square · 2025Article
- Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025Review
- APOBEC3A deaminates CTG hairpin loops to promote fragility and instability of expanded CAG/CTG repeats.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024Review
- Hypomorphic mutation in the large subunit of replication protein A affects mutagenesis by human APOBEC cytidine deaminases in yeast.G3 (Bethesda, Md.) · 2024Article
- Stressed? Break-induced replication comes to the rescue!DNA repair · 2024Review
- The SMC5/6 complex prevents genotoxicity upon APOBEC3A-mediated replication stress.The EMBO journal · 2024Article
- Hypomorphic mutation in the large subunit of replication protein A affects mutagenesis by human APOBEC cytidine deaminases in yeast.bioRxiv : the preprint server for biology · 2024Article
- Kataegis associated mutational processes linked to adverse prostate cancer presentation in African men.Research square · 2024Article
- Splitting the yeast centromere by recombination.Nucleic acids research · 2024Article
- Telomere-related DNA damage response pathways in cancer therapy: prospective targets.Frontiers in pharmacology · 2024Review
- Viral infection, APOBEC3 dysregulation, and cancer.Frontiers in genetics · 2024Review
- Meiotic DNA breaks drive multifaceted mutagenesis in the human germ line.Science (New York, N.Y.) · 2023Article
- Article
- Transcriptional and genetic alterations of cuproptosis-related genes correlated to malignancy and immune-infiltrate of esophageal carcinoma.Cell death discovery · 2022Article
- Break-induced replication: unraveling each step.Trends in genetics : TIG · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Break induced replication (BIR) is a double strand break repair pathway that can promote genetic instabilities similar to those observed in cancer. Instead of a replication fork, BIR is driven by a migration bubble where asynchronous synthesis between leading and lagging strands leads to accumulation of single-stranded DNA (ssDNA) that promotes mutation. However, the details of the mechanism of mutagenesis, including the identity of the participating proteins, remain unknown. Using yeast as a model, we demonstrate that mutagenic ssDNA is formed at multiple positions along the BIR track and that Pol ζ is responsible for the majority of both spontaneous and damage-induced base substitutions during BIR. We also report that BIR creates a potent substrate for APOBEC3A (A3A) cytidine deaminase that can promote formation of mutation clusters along the entire track of BIR. Finally, we demonstrate that uracil glycosylase initiates the bypass of DNA damage induced by A3A in the context of BIR without formation of base substitutions, but instead this pathway frequently leads to chromosomal rearrangements. Together, the expression of A3A during BIR in yeast recapitulates the main features of APOBEC-induced kataegis in human cancers, suggesting that BIR might represent an important source of these hyper-mutagenic events.
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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.