ArticleGenetics2007
Drosophila ATR in double-strand break repair.
Article in Genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 70 citations in OpenAlex.
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- Replication stress promotes cellular transformation in Drosophila epithelium.Cell death discovery · 2025Article
- Emerin preserves stem cell survival through maintenance of centrosome and nuclear lamina structure.Development (Cambridge, England) · 2024Article
- Double-strand breaks in facultative heterochromatin require specific movements and chromatin changes for efficient repair.Nature communications · 2024Article
- Article
- HR repair pathway plays a crucial role in maintaining neural stem cell fate under irradiation stress.Life science alliance · 2023Article
- Mutation and apoptosis are well-coordinated for protecting against DNA damage-inducing toxicity in Drosophila.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023Article
- Analysis of a rare progeria variant of Barrier-to-autointegration factor in Drosophila connects centromere function to tissue homeostasis.Cellular and molecular life sciences : CMLS · 2023Article
- Structure-function analysis of Cdc25Fly · 2022Article
- Phosphorylated histone variant γH2Av is associated with chromatin insulators in Drosophila.PLoS genetics · 2022Article
- Checkpoint activation drives global gene expression changes in Drosophila nuclear lamina mutants.G3 (Bethesda, Md.) · 2022Article
- Taming active transposons at Drosophila telomeres: The interconnection between HipHop's roles in capping and transcriptional silencing.PLoS genetics · 2021Article
- ATR prevents CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Drosophila female germline stem cells undergo mitosis without nuclear breakdown.Current biology : CB · 2021Article
- Analysis of ovarian transcriptomes reveals thousands of novel genes in the insect vector Rhodnius prolixus.Scientific reports · 2021Article
- Mutations in the insulator protein Suppressor of Hairy wing induce genome instability.Chromosoma · 2020Article
- What Drosophila Can Teach Us About Radiation Biology of Human Cancers.Advances in experimental medicine and biology · 2019Review
- Loss ofGenetics · 2018Article
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
The ability of a cell to sense and respond to DNA damage is essential for genome stability. An important aspect of the response is arrest of the cell cycle, presumably to allow time for repair. Ataxia telangiectasia mutated (ATM) and ATR are essential for such cell-cycle control, but some observations suggest that they also play a direct role in DNA repair. The Drosophila ortholog of ATR, MEI-41, mediates the DNA damage-dependent G2-M checkpoint. We examined the role of MEI-41 in repair of double-strand breaks (DSBs) induced by P-element excision. We found that mei-41 mutants are defective in completing the later steps of homologous recombination repair, but have no defects in end-joining repair. We hypothesized that these repair defects are the result of loss of checkpoint control. To test this, we genetically reduced mitotic cyclin levels and also examined repair in grp (DmChk1) and lok (DmChk2) mutants. Our results suggest that a significant component of the repair defects is due to loss of MEI-41-dependent cell cycle regulation. However, this does not account for all of the defects we observed. We propose a novel role for MEI-41 in DSB repair, independent of the Chk1/Chk2-mediated checkpoint response.
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What OpenQuestion holds
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.