ReviewCell cycle (Georgetown, Tex.)2018
Control of meiotic double-strand-break formation by ATM: local and global views.
Review in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 41 citations in OpenAlex.
- ATM/p53-Associated Apoptosis Contributes to Sterility in Allotriploid Crucian Carp.Animals : an open access journal from MDPI · 2026Article
- MRE11 suppresses germline mutagenesis at meiotic double-strand breaks in mice.Genes & development · 2026Article
- Crossover control: A key to unlocking genetic diversity in plant breeding.Journal of integrative plant biology · 2026Review
- Critical roles of MCM8 in meiotic recombination during mouse spermatogenesis.bioRxiv : the preprint server for biology · 2026Article
- MRE11 suppresses germline mutagenesis at meiotic double-strand breaks in mice.bioRxiv : the preprint server for biology · 2026Article
- Mutual, spatially limited control of meiotic DNA break formation by Mre11-Rad50-Nbs1 DNA repair complex and Tel1 (ATM) protein kinase.Nucleic acids research · 2025Article
- Tel1 is recruited at chromosomal loop/axis contact sites to modulate meiotic DNA double-strand breaks interference.PLoS genetics · 2025Article
- Loss of meiotic double strand breaks triggers recruitment of recombination-independent pro-crossover factors in C. elegans spermatogenesis.PLoS genetics · 2025Article
- Insight into meiotic DNA end resection: Mechanisms and regulation.DNA repair · 2025Review
- Mouse MRE11-RAD50-NBS1 is needed to start and extend meiotic DNA end resection.Nature communications · 2025Article
- Keeping it safe: control of meiotic chromosome breakage.Trends in genetics : TIG · 2025Review
- Meiotic prophase length modulates Tel1-dependent DNA double-strand break interference.PLoS genetics · 2024Article
- Methods of Detection and Mechanisms of Origin of Complex Structural Genome Variations.Methods in molecular biology (Clifton, N.J.) · 2024Review
- RNase H1 facilitates recombinase recruitment by degrading DNA-RNA hybrids during meiosis.Nucleic acids research · 2023Article
- Article
- SCF ubiquitin E3 ligase regulates DNA double-strand breaks in early meiotic recombination.Nucleic acids research · 2022Article
- Article
- Conservation and divergence of meiotic DNA double strand break forming mechanisms in Arabidopsis thaliana.Nucleic acids research · 2021Article
- ATM controls meiotic DNA double-strand break formation and recombination and affects synaptonemal complex organization in plants.The Plant cell · 2021Article
- HIM-17 regulates the position of recombination events and GSP-1/2 localization to establish short arm identity on bivalents in meiosis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
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 1 institution in 1 country.
Funding
Abstract
DNA double-strand breaks (DSBs) generated by the SPO11 protein initiate meiotic recombination, an essential process for successful chromosome segregation during gametogenesis. The activity of SPO11 is controlled by multiple factors and regulatory mechanisms, such that the number of DSBs is limited and DSBs form at distinct positions in the genome and at the right time. Loss of this control can affect genome integrity or cause meiotic arrest by mechanisms that are not fully understood. Here we focus on the DSB-responsive kinase ATM and its functions in regulating meiotic DSB numbers and distribution. We review the recently discovered roles of ATM in this context, discuss their evolutionary conservation, and examine future research perspectives.
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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.