ArticlePLoS genetics2012
Competition between replicative and translesion polymerases during homologous recombination repair in Drosophila.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 56 citations in OpenAlex.
- POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024Review
- REV1 coordinates a multi-faceted tolerance response to DNA alkylation damage and prevents chromosome shattering in Drosophila melanogaster.PLoS genetics · 2024Article
- Association of Mutations in Replicative DNA Polymerase Genes with Human Disease: Possible Application ofInternational journal of molecular sciences · 2023Review
- Changes in the architecture and abundance of replication intermediates delineate the chronology of DNA damage tolerance pathways at UV-stalled replication forks in human cells.Nucleic acids research · 2022Article
- Host translesion polymerases are required for viral genome integrity.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Division of Labor by the HELQ, BLM, and FANCM Helicases during Homologous Recombination Repair inGenes · 2022Article
- Take a Break to Repair: A Dip in the World of Double-Strand Break Repair Mechanisms Pointing the Gaze on Archaea.International journal of molecular sciences · 2021Review
- DNA polymerase zeta contributes to heterochromatin replication to prevent genome instability.The EMBO journal · 2021Article
- Episodes of Rapid Recovery of the Functional Activity of theFrontiers in genetics · 2021Article
- Review
- Genetic mechanisms of formation of radiation-induced instability of the genome and its transgenerational effects in the descendants of chronically irradiated individuals of Drosophila melanogaster.Radiation and environmental biophysics · 2020Article
- Mechanisms of genome evolution in Candida albicans.Current opinion in microbiology · 2019Review
- TheGenetics · 2019Article
- DNA double-strand break repair-pathway choice in somatic mammalian cells.Nature reviews. Molecular cell biology · 2019Review
- Article
- The processivity factor Pol32 mediates nuclear localization of DNA polymerase delta and prevents chromosomal fragile site formation in Drosophila development.PLoS genetics · 2019Article
- Transcriptome profiling of aging Drosophila photoreceptors reveals gene expression trends that correlate with visual senescence.BMC genomics · 2017Article
- Break-induced replication links microsatellite expansion to complex genome rearrangements.BioEssays : news and reviews in molecular, cellular and developmental biology · 2017Review
- Review
- Multiple mechanisms contribute to double-strand break repair at rereplication forks in Drosophila follicle cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
In metazoans, the mechanism by which DNA is synthesized during homologous recombination repair of double-strand breaks is poorly understood. Specifically, the identities of the polymerase(s) that carry out repair synthesis and how they are recruited to repair sites are unclear. Here, we have investigated the roles of several different polymerases during homologous recombination repair in Drosophila melanogaster. Using a gap repair assay, we found that homologous recombination is impaired in Drosophila lacking DNA polymerase zeta and, to a lesser extent, polymerase eta. In addition, the Pol32 protein, part of the polymerase delta complex, is needed for repair requiring extensive synthesis. Loss of Rev1, which interacts with multiple translesion polymerases, results in increased synthesis during gap repair. Together, our findings support a model in which translesion polymerases and the polymerase delta complex compete during homologous recombination repair. In addition, they establish Rev1 as a crucial factor that regulates the extent of repair synthesis.
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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.