ArticleNature2014
Homologue engagement controls meiotic DNA break number and distribution.
Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 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.
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
143 citing papers in PubMed, 221 citations in OpenAlex.
- Separable downmodulation of meiotic axis protein deposition and DNA break induction at chromosome ends.eLife · 2026Article
- RMI2 regulates recombination intermediate metabolism to ensure proper chromosome segregation in mammalian meiosis.Nucleic acids research · 2026Article
- The HORMA-domain protein ASY1 recruits the plant-specific cyclin SDS to promote DMC1-mediated meiotic recombination.The Plant cell · 2026Article
- Structure and function of the synaptonemal complex.The Journal of cell biology · 2026Review
- Directional branch migration remodels the meiotic Holliday junction landscape.bioRxiv : the preprint server for biology · 2026Article
- Mei4 deficiency induces sexual dimorphism in early meiosis and promotes production of unreduced eggs in zebrafish.Zoological research · 2026Article
- Mms4 chromosomal association reveals functional relationships between meiotic crossover pathways in budding yeast.PLoS genetics · 2026Article
- Article
- BAF-1-VRK-1 mediated release of meiotic chromosomes from the nuclear periphery is important for genome integrity.Nature communications · 2025Article
- Mismatch repair disturbs meiotic crossover control in S. cerevisiae.Nucleic acids research · 2025Article
- Article
- Crossover designation recruits condensin to reorganize the meiotic chromosome axis.Current biology : CB · 2025Article
- Crossover designation recruits condensin to reorganize the meiotic chromosome axis.bioRxiv : the preprint server for biology · 2025Article
- Insight into meiotic DNA end resection: Mechanisms and regulation.DNA repair · 2025Review
- Article
- Improved synapsis dynamics accompany meiotic stability inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Keeping it safe: control of meiotic chromosome breakage.Trends in genetics : TIG · 2025Review
- The ATPase activity of yeast chromosome axis protein Hop1 affects the frequency of meiotic crossovers.Nucleic acids research · 2025Article
- Separable roles of the DNA damage response kinase Mec1ATR and its activator Rad24RAD17 during meiotic recombination.PLoS genetics · 2024Article
- Seeding the meiotic DNA break machinery and initiating recombination on chromosome axes.Nature communications · 2024Article
83 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Meiotic recombination promotes genetic diversification as well as pairing and segregation of homologous chromosomes, but the double-strand breaks (DSBs) that initiate recombination are dangerous lesions that can cause mutation or meiotic failure. How cells control DSBs to balance between beneficial and deleterious outcomes is not well understood. Here we test the hypothesis that DSB control involves a network of intersecting negative regulatory circuits. Using multiple complementary methods, we show that DSBs form in greater numbers in Saccharomyces cerevisiae cells lacking ZMM proteins, a suite of recombination-promoting factors traditionally regarded as acting strictly downstream of DSB formation. ZMM-dependent DSB control is genetically distinct from a pathway tying break formation to meiotic progression through the Ndt80 transcription factor. These counterintuitive findings suggest that homologous chromosomes that have successfully engaged one another stop making breaks. Genome-wide DSB maps uncover distinct responses by different subchromosomal domains to the ZMM mutation zip3 (also known as cst9), and show that Zip3 is required for the previously unexplained tendency of DSB density to vary with chromosome size. Thus, feedback tied to ZMM function contributes in unexpected ways to spatial patterning of 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.