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- W2154762186 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." @default.
- W2154762186 created "2016-06-24" @default.
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- W2154762186 date "2012-04-19" @default.
- W2154762186 modified "2023-09-27" @default.
- W2154762186 title "Competition between Replicative and Translesion Polymerases during Homologous Recombination Repair in Drosophila" @default.
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- W2154762186 doi "https://doi.org/10.1371/journal.pgen.1002659" @default.
- W2154762186 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3330096" @default.
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