ArticleScience advances2020
Sexual dimorphism in the meiotic requirement for PRDM9: A mammalian evolutionary safeguard.
Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- On the origin of PRDM9-guided recombination hotspots.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dynamic regulation of spermatogenesis and hybrid sterility revealed by single-cell analysis in yak and cattle.Molecular biology and evolution · 2026Article
- Heterozygous PRDM9 truncating variant in a patient with primary ovarian insufficiency.Journal of human genetics · 2025Article
- Investigation and design of the dual specificity of the PRDM9 protein lysine methyltransferase.Communications biology · 2025Article
- Single-cell and bulk transcriptional profiling of mouse ovaries reveals novel genes and pathways associated with DNA damage response in oocytes.Developmental biology · 2025Article
- Checkpoint kinase 2 controls insulin secretion and glucose homeostasis.Nature chemical biology · 2024Article
- Meiosis through three centuries.Chromosoma · 2024Review
- Patterns of recombination in snakes reveal a tug-of-war between PRDM9 and promoter-like features.Science (New York, N.Y.) · 2024Article
- Single-cell and bulk transcriptional profiling of mouse ovaries reveals novel genes and pathways associated with DNA damage response in oocytes.bioRxiv : the preprint server for biology · 2024Article
- Hypoxia Inducible Factors (HIF1α and HIF3α) are differentially methylated in preeclampsia placentae and are associated with birth outcomes.Molecular and cellular biochemistry · 2023Article
- Reproductive genomics of the mouse: implications for human fertility and infertility.Development (Cambridge, England) · 2023Article
- Prdm9 deficiency of rat oocytes causes synapsis among non-homologous chromosomes and aneuploidy.Mammalian genome : official journal of the International Mammalian Genome Society · 2022Article
- Using the Collaborative Cross and Diversity Outbred Mice in Immunology.Current protocols · 2022Article
- Differential effects of two catalytic mutations on full-length PRDM9 and its isolated PR/SET domain reveal a case of pseudomodularity.Genetics · 2021Article
- Pathogenic variants of meiotic double strand break (DSB) formation genes PRDM9 and ANKRD31 in premature ovarian insufficiency.Genetics in medicine : official journal of the American College of Medical Genetics · 2021Article
- Higher Intercellular Variation in Genome-Wide Recombination Rate in Female Mice.Cytogenetic and genome research · 2021Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
In many mammals, genomic sites for recombination are determined by the histone methyltransferase PRMD9. Some mouse strains lacking PRDM9 are infertile, but instances of fertility or semifertility in the absence of PRDM9 have been reported in mice, canines, and a human female. Such findings raise the question of how the loss of PRDM9 is circumvented to maintain fertility. We show that genetic background and sex-specific modifiers can obviate the requirement for PRDM9 in mice. Specifically, the meiotic DNA damage checkpoint protein CHK2 acts as a modifier allowing female-specific fertility in the absence of PRDM9. We also report that, in the absence of PRDM9, a PRDM9-independent recombination system is compatible with female meiosis and fertility, suggesting sex-specific regulation of meiotic recombination, a finding with implications for speciation.
Identifiers
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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.