ArticlePLoS genetics2012
Interallelic and intergenic incompatibilities of the Prdm9 (Hst1) gene in mouse hybrid sterility.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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51 citing papers in PubMed, 80 citations in OpenAlex.
- Molecular assessment of recombination processing across genetically diverse mouse strains reveals sexually dimorphic determinants of crossover distribution beyond chromosome length.Molecular biology and evolution · 2026Article
- Beyond the Prdm9 model: independent evolution of hybrid male sterility in house mice.Heredity · 2026Article
- Epigenetic regulation by DNA methylation, histone modifications and chromatin remodeling complexes in controlling spermatogenesis and their dysfunction with male infertility.Cellular and molecular life sciences : CMLS · 2025Review
- Functional test of a naturally occurred tumor modifier gene provides insights to melanoma development.G3 (Bethesda, Md.) · 2025Article
- PRDM9 drives the location and rapid evolution of recombination hotspots in salmonid fish.PLoS biology · 2025Article
- Natural variation in the zinc-finger-encoding exon of Prdm9 affects hybrid sterility phenotypes in mice.Genetics · 2024Article
- Down the Penrose stairs, or how selection for fewer recombination hotspots maintains their existence.eLife · 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
- Two Loci Contribute to Age-Related Hearing Loss Resistance in the Japanese Wild-Derived Inbred MSM/Ms Mice.Biomedicines · 2022Article
- Stage-specific disruption of X chromosome expression during spermatogenesis in sterile house mouse hybrids.G3 (Bethesda, Md.) · 2022Article
- Rat PRDM9 shapes recombination landscapes, duration of meiosis, gametogenesis, and age of fertility.BMC biology · 2021Article
- Article
- Cataloging HumanFrontiers in cell and developmental biology · 2021Article
- Oncogenic allelic interaction inProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- Copy-number variation introduced by long transgenes compromises mouse male fertility independently of pachytene checkpoints.Chromosoma · 2020Article
- Genomic Structure ofGenetics · 2019Article
- PRDM9 Diversity at Fine Geographical Scale Reveals Contrasting Evolutionary Patterns and Functional Constraints in Natural Populations of House Mice.Molecular biology and evolution · 2019Article
- PRDM9 forms a trimer by interactions within the zinc finger array.Life science alliance · 2019Article
- Histone methyltransferase PRDM9 is not essential for meiosis in male mice.Genome research · 2019Article
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Authors and funding
11 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Dobzhansky-Muller model of incompatibilities explains reproductive isolation between species by incorrect epistatic interactions. Although the mechanisms of speciation are of great interest, no incompatibility has been characterized at the gene level in mammals. The Hybrid sterility 1 gene (Hst1) participates in the arrest of meiosis in F(1) males of certain strains from two Mus musculus subspecies, e.g., PWD from M. m. musculus and C57BL/6J (henceforth B6) from M. m. domesticus. Hst1 has been identified as a meiotic PR-domain gene (Prdm9) encoding histone 3 methyltransferase in the male offspring of PWD females and B6 males, (PWD×B6)F(1). To characterize the incompatibilities underlying hybrid sterility, we phenotyped reproductive and meiotic markers in males with altered copy numbers of Prdm9. A partial rescue of fertility was observed upon removal of the B6 allele of Prdm9 from the azoospermic (PWD×B6)F(1) hybrids, whereas removing one of the two Prdm9 copies in PWD or B6 background had no effect on male reproduction. Incompatibility(ies) not involving Prdm9(B6) also acts in the (PWD×B6)F(1) hybrids, since the correction of hybrid sterility by Prdm9(B6) deletion was not complete. Additions and subtractions of Prdm9 copies, as well as allelic replacements, improved meiotic progression and fecundity also in the progeny-producing reciprocal (B6×PWD)F(1) males. Moreover, an increased dosage of Prdm9 and reciprocal cross enhanced fertility of other sperm-carrying male hybrids, (PWD×B6-C3H.Prdm9)F(1), harboring another Prdm9 allele of M. m. domesticus origin. The levels of Prdm9 mRNA isoforms were similar in the prepubertal testes of all types of F(1) hybrids of PWD with B6 and B6-C3H.Prdm9 despite their different prospective fertility, but decreased to 53% after removal of Prdm9(B6). Therefore, the Prdm9(B6) allele probably takes part in posttranscriptional dominant-negative hybrid interaction(s) absent in the parental strains.
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