ArticleJournal of reproductive immunology2024
Individual disruption of 12 testis-enriched genes via the CRISPR/Cas9 system does not affect the fertility of male mice.
Article in Journal of reproductive immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- Review
- The Cilia-Associated Protein CCDC89 Is Dispensable for Male Fertility in Mice.Cytoskeleton (Hoboken, N.J.) · 2026Article
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- Sperm activation for fertilization requires robust activity of the TAT-5 lipid flippase.Developmental biology · 2025Article
- Analysis of Transcript Expression and Core Promoter DNA Sequences of Brain, Adipose Tissues and Testis in Human and Fruit Fly.International journal of molecular sciences · 2025Article
- Tdrd15 is dispensable for male fertility and spermatogenesis in the golden hamster.European journal of medical research · 2025Article
- Genome Editing for Fertility: Unlocking the Promise of CRISPR/Cas9 in Addressing Male Infertility - A Narrative Review.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Proximity labeling of axonemal protein CFAP91 identifies EFCAB5 that regulates sperm motility.Nature communications · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
More than 1200 genes have been shown in the database to be expressed predominantly in the mouse testes. Advances in genome editing technologies such as the CRISPR/Cas9 system have made it possible to create genetically engineered mice more rapidly and efficiently than with conventional methods, which can be utilized to screen genes essential for male fertility by knocking out testis-enriched genes. Finding such genes related to male fertility would not only help us understand the etiology of human infertility but also lead to the development of male contraceptives. In this study, we generated knockout mice for 12 genes (Acrv1, Adgrf3, Atp8b5, Cfap90, Cfap276, Fbxw5, Gm17266, Lrrd1, Mroh7, Nemp1, Spata45, and Trim36) that are expressed predominantly in the testis and examined the appearance and histological morphology of testes, sperm motility, and male fertility. Mating tests revealed that none of these genes is essential for male fertility at least individually. Notably, knockout mice for Gm17266 showed smaller testis size than the wild-type but did not exhibit reduced male fertility. Since 12 genes were not individually essential for male fertilization, it is unlikely that these genes could be the cause of infertility or contraceptive targets. It is better to focus on other essential genes because complementary genes to these 12 genes may exist.
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Registered trials
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