ArticleNature2016
Re-engineering the zinc fingers of PRDM9 reverses hybrid sterility in mice.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 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
134 citing papers in PubMed, 227 citations in OpenAlex.
- PRDM9-mediated meiotic hotspot specification is constrained in humans despite extensive sequence diversity.bioRxiv : the preprint server for biology · 2026Article
- Mapping Meiotic Recombination DNA Double-Strand Breaks (DSBs) Hotspots -Methodological Advances and Challenges.Advanced genetics (Hoboken, N.J.) · 2026Article
- The Role of theGenes · 2026Article
- On the origin of PRDM9-guided recombination hotspots.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- XPF-like domain in human SHOC1 is required for crossover formation and protecting autosome from MSUC.Nucleic acids research · 2026Article
- Why recombination hotspots?PLoS genetics · 2026Review
- Beyond the Prdm9 model: independent evolution of hybrid male sterility in house mice.Heredity · 2026Article
- Divergent Amplification of Y-Linked Dosage-Sensitive Genes Triggers Regulatory Mismatch Underlying Cattle-Yak Male Sterility.Biomolecules · 2026Article
- Dynamic regulation of spermatogenesis and hybrid sterility revealed by single-cell analysis in yak and cattle.Molecular biology and evolution · 2026Article
- Mechanism and potential therapeutic strategies of genetic abnormalities involved in deoxyribonucleic acid double-strand breaks leading to the development of human non-obstructive azoospermia.Reproductive biology and endocrinology : RB&E · 2026Review
- G-quadruplex structures are key regulators of mammalian spermatogenesis.Cellular & molecular biology letters · 2026Article
- Mouse X-linked microRNA cluster regulates the meiotic checkpoint andProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Phenogenomic resources immortalized in a panel of wild-derived strains of five species of house mice.Scientific reports · 2025Article
- Characterization of PRDM9 Multifunctionality in Yak Testes Through Protein Interaction Mapping.International journal of molecular sciences · 2025Article
- Different complex regulatory phenotypes underlie hybrid male sterility in divergent rodent crosses.Genetics · 2025Article
- PRDM9 drives the location and rapid evolution of recombination hotspots in salmonid fish.PLoS biology · 2025Article
- Different complex regulatory phenotypes underlie hybrid male sterility in divergent rodent crosses.bioRxiv : the preprint server for biology · 2024Article
- A Minimal Hybrid Sterility Genome Assembled by Chromosome Swapping Between Mouse Subspecies (Mus musculus).Molecular biology and evolution · 2024Article
- FIGNL1-FIRRM is essential for meiotic recombination and prevents DNA damage-independent RAD51 and DMC1 loading.Nature communications · 2024Article
- Understanding the Genetic Basis of Variation in Meiotic Recombination: Past, Present, and Future.Molecular biology and evolution · 2024Review
74 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
Abstract
The DNA-binding protein PRDM9 directs positioning of the double-strand breaks (DSBs) that initiate meiotic recombination in mice and humans. Prdm9 is the only mammalian speciation gene yet identified and is responsible for sterility phenotypes in male hybrids of certain mouse subspecies. To investigate PRDM9 binding and its role in fertility and meiotic recombination, we humanized the DNA-binding domain of PRDM9 in C57BL/6 mice. This change repositions DSB hotspots and completely restores fertility in male hybrids. Here we show that alteration of one Prdm9 allele impacts the behaviour of DSBs controlled by the other allele at chromosome-wide scales. These effects correlate strongly with the degree to which each PRDM9 variant binds both homologues at the DSB sites it controls. Furthermore, higher genome-wide levels of such 'symmetric' PRDM9 binding associate with increasing fertility measures, and comparisons of individual hotspots suggest binding symmetry plays a downstream role in the recombination process. These findings reveal that subspecies-specific degradation of PRDM9 binding sites by meiotic drive, which steadily increases asymmetric PRDM9 binding, has impacts beyond simply changing hotspot positions, and strongly support a direct involvement in hybrid infertility. Because such meiotic drive occurs across mammals, PRDM9 may play a wider, yet transient, role in the early stages of speciation.
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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.