ArticleGenetics2007
A genetic screen for DNA double-strand break repair mutations in Drosophila.
Article in Genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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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Who cites it
38 citing papers in PubMed, 50 citations in OpenAlex.
- The epistatic relationship of Drosophila melanogaster CtIP and Rif1 in homology-directed repair of DNA double-strand breaks.G3 (Bethesda, Md.) · 2024Article
- The effect of repeat length on Marcal1-dependent single-strand annealing in Drosophila.Genetics · 2023Article
- Gene drives gaining speed.Nature reviews. Genetics · 2022Review
- Helicase Q promotes homology-driven DNA double-strand break repair and prevents tandem duplications.Nature communications · 2021Article
- The Role ofGenes · 2021Article
- Article
- CopyCatchers are versatile active genetic elements that detect and quantify inter-homolog somatic gene conversion.Nature communications · 2021Article
- DNA polymerase theta suppresses mitotic crossing over.PLoS genetics · 2021Article
- spn-A/rad51 mutant exhibits enhanced genomic damage, cell death and low temperature sensitivity in somatic tissues.Chromosoma · 2021Article
- Episodes of Rapid Recovery of the Functional Activity of theFrontiers in genetics · 2021Article
- Active Genetic Neutralizing Elements for Halting or Deleting Gene Drives.Molecular cell · 2020Article
- The processivity factor Pol32 mediates nuclear localization of DNA polymerase delta and prevents chromosomal fragile site formation in Drosophila development.PLoS genetics · 2019Article
- Efficient allelic-drive in Drosophila.Nature communications · 2019Article
- Article
- Secondary structure forming sequences drive SD-MMEJ repair of DNA double-strand breaks.Nucleic acids research · 2017Article
- The Role of Blm Helicase in Homologous Recombination, Gene Conversion Tract Length, and Recombination Between Diverged Sequences inGenetics · 2017Article
- Aging impairs double-strand break repair by homologous recombination in Drosophila germ cells.Aging cell · 2017Article
- Article
- Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The study of DNA double-strand break (DSB) repair has been greatly facilitated by the use of rare-cutting endonucleases, which induce a break precisely at their cut sites that can be strategically placed in the genome. We previously established such a system in Drosophila and showed that the yeast I-SceI enzyme cuts efficiently in Drosophila cells and those breaks are effectively repaired by conserved mechanisms. In this study, we determined the genetic requirements for the repair of this I-SceI-induced DSB in the germline. We show that Drosophila Rad51 and Rad54 are both required for homologous repair by gene conversion, but are dispensable for single-strand annealing repair. We provided evidence suggesting that Rad51 is more stringently required than Rad54 for intersister gene conversion. We uncovered a significant role of DNA ligase IV in nonhomologous end joining. We conducted a screen for candidate mutations affecting DSB repair and discovered novel mutations in genes that include mutagen sensitive 206, single-strand annealing reducer, and others. In addition, we demonstrated an intricate balance among different repair pathways in which the cell differentially utilizes repair mechanisms in response to both changes in the genomic environment surrounding the break and deficiencies in one or the other repair pathways.
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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.