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- W2065912182 abstract "P transposable elements in Drosophila are mobilized via a cut-and-paste mechanism. The broken DNA ends generated during transposition can be repaired via the homology-directed synthesis-dependent strand annealing or by nonhomologous end joining (NHEJ). Genetic studies have demonstrated an interaction between the gene (mus309, for mutagen-sensitive) encoding the Drosophila Bloom's syndrome helicase homolog (DmBLM) and the Ku70 gene, which is involved in NHEJ. We have used RNA interference (RNAi) to knock down expression of DmBLM and one or both of the Drosophila Ku subunits, DmKu70 or DmKu80. Our results show that upon reduction of DmKu, an increase in small deletions (1-49 bp) and large deletions (>/=50 bp) flanking the site of P element-induced breaks is observed, and a reduction in large deletions at these sites is found upon reduction of DmBLM. Moreover, double RNAi of DmKu and DmBLM results in an increase in small deletions characteristic of the DmKu RNAi and also partially suppresses the reduction in repair efficiency observed with DmKu RNAi. These results suggest that there are DNA double-strand break recognition and/or processing events involving DmKu and DmBLM that, when eliminated by RNAi, lead to deletions. Finally, these results raise the possibility that, unlike the situation in mammals, where BLM appears to function exclusively in the homologous repair pathway, in Drosophila, DmBLM may be directly involved in, or at least influence the double-strand break recognition that leads to the NHEJ repair pathway." @default.
- W2065912182 created "2016-06-24" @default.
- W2065912182 creator A5031742485 @default.
- W2065912182 creator A5034073565 @default.
- W2065912182 creator A5074542763 @default.
- W2065912182 date "2004-06-07" @default.
- W2065912182 modified "2023-09-23" @default.
- W2065912182 title "Interplay between <i>Drosophila</i> Bloom's syndrome helicase and Ku autoantigen during nonhomologous end joining repair of <i>P</i> element-induced DNA breaks" @default.
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- W2065912182 doi "https://doi.org/10.1073/pnas.0403000101" @default.
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