ArticleGenetics2022
Genic and chromosomal components of Prdm9-driven hybrid male sterility in mice (Mus musculus).
Article in Genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 10 citations in OpenAlex.
- 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
- A Minimal Hybrid Sterility Genome Assembled by Chromosome Swapping Between Mouse Subspecies (Mus musculus).Molecular biology and evolution · 2024Article
- Do genetic loci that cause reproductive isolation in the lab inhibit gene flow in nature?Evolution; international journal of organic evolution · 2024Article
- Natural variation in the zinc-finger-encoding exon of Prdm9 affects hybrid sterility phenotypes in mice.Genetics · 2024Article
- Meiotic Recognition of Evolutionarily Diverged Homologs: Chromosomal Hybrid Sterility Revisited.Molecular biology and evolution · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hybrid sterility contributes to speciation by preventing gene flow between related taxa. Prdm9, the first and only hybrid male sterility gene known in vertebrates, predetermines the sites of recombination between homologous chromosomes and their synapsis in early meiotic prophase. The asymmetric binding of PRDM9 to heterosubspecific homologs of Mus musculus musculus × Mus musculus domesticus F1 hybrids and increase of PRDM9-independent DNA double-strand break hotspots results indificult- to- repair double-strand breaks, incomplete synapsis of homologous chromosomes, and meiotic arrest at the first meiotic prophase. Here, we show that Prdm9 behaves as a major hybrid male sterility gene in mice outside the Mus musculus musculus × Mus musculus domesticus F1 hybrids, in the genomes composed of Mus musculus castaneus and Mus musculus musculus chromosomes segregating on the Mus musculus domesticus background. The Prdm9cst/dom2 (castaneus/domesticus) allelic combination secures meiotic synapsis, testes weight, and sperm count within physiological limits, while the Prdm9msc1/dom2 (musculus/domesticus) males show a range of fertility impairment. Out of 5 quantitative trait loci contributing to the Prdm9msc1/dom2-related infertility, 4 control either meiotic synapsis or fertility phenotypes and 1 controls both, synapsis, and fertility. Whole-genome genotyping of individual chromosomes showed preferential involvement of nonrecombinant musculus chromosomes in asynapsis in accordance with the chromosomal character of hybrid male sterility. Moreover, we show that the overall asynapsis rate can be estimated solely from the genotype of individual males by scoring the effect of nonrecombinant musculus chromosomes. Prdm9-controlled hybrid male sterility represents an example of genetic architecture of hybrid male sterility consisting of genic and chromosomal components.
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