ArticleNucleic acids research2022
Redirecting meiotic DNA break hotspot determinant proteins alters localized spatial control of DNA break formation and repair.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 7 citations in OpenAlex.
- 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
- Keeping it safe: control of meiotic chromosome breakage.Trends in genetics : TIG · 2025Review
- Mug20-Rec25-Rec27 binds DNA and enhances meiotic DNA break formation via phase-separated condensates.Nucleic acids research · 2025Article
- The plant early recombinosome: a high security complex to break DNA during meiosis.Plant reproduction · 2024Review
- Meiotic chromosome organization and its role in recombination and cancer.Current topics in developmental biology · 2023Review
- Meiotic crossover interference: Methods of analysis and mechanisms of action.Current topics in developmental biology · 2023Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
During meiosis, DNA double-strand breaks (DSBs) are formed at high frequency at special chromosomal sites, called DSB hotspots, to generate crossovers that aid proper chromosome segregation. Multiple chromosomal features affect hotspot formation. In the fission yeast S. pombe the linear element proteins Rec25, Rec27 and Mug20 are hotspot determinants - they bind hotspots with high specificity and are necessary for nearly all DSBs at hotspots. To assess whether they are also sufficient for hotspot determination, we localized each linear element protein to a novel chromosomal site (ade6 with lacO substitutions) by fusion to the Escherichia coli LacI repressor. The Mug20-LacI plus lacO combination, but not the two separate lac elements, produced a strong ade6 DSB hotspot, comparable to strong endogenous DSB hotspots. This hotspot had unexpectedly low ade6 recombinant frequency and negligible DSB hotspot competition, although like endogenous hotspots it manifested DSB interference. We infer that linear element proteins must be properly placed by endogenous functions to impose hotspot competition and proper partner choice for DSB repair. Our results support and expand our previously proposed DSB hotspot-clustering model for local control of meiotic recombination.
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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.