ArticleBiology of reproduction2019
CRISPR/Cas9-mediated genome editing reveals 30 testis-enriched genes dispensable for male fertility in mice†.
Article in Biology of reproduction, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
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Who cites it
74 citing papers in PubMed, 118 citations in OpenAlex.
- Loss-of-Function SSFA2 Variants Disrupt Fertility Through Impaired Acrosome Formation and Sperm Function.Andrology · 2026Article
- CRISPR/Cas9-mediated genome editing identifies six testis-expressed genes individually dispensable for overt male fecundity in mice.Journal of biomedical research · 2026Article
- Bioinformatics and multi-omics approaches in male infertility: implications for diagnosis and assisted reproduction.Journal of assisted reproduction and genetics · 2026Review
- Molecular interplay between sperm and oocyte: a narrative review.Human reproduction update · 2026Review
- C2orf74 orchestrates germ-Leydig crosstalk to inhibit white adipose tissue browning in male mice.Nature communications · 2026Article
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- Chromosomal Roadblocks in Male Fertility: Mechanisms, Risk Factors and Syndromes.Medicina (Kaunas, Lithuania) · 2025Review
- Genome Editing for Fertility: Unlocking the Promise of CRISPR/Cas9 in Addressing Male Infertility - A Narrative Review.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Sexual selection and pseudogenization in primate fertilization.Evolution; international journal of organic evolution · 2025Article
- SLC35G3 is a UDP-N-acetylglucosamine transporter for sperm glycoprotein formation and underpins male fertility in mice.bioRxiv : the preprint server for biology · 2025Article
- L-2-hydroxyglutarate regulates centromere and heterochromatin conformation in the male germline.PLoS genetics · 2025Article
- Age-Associated Proteomic Changes in Human Spermatozoa.International journal of molecular sciences · 2025Article
- Expression of Random Sequences and de novo Evolved Genes From the Mouse in Human Cells Reveals Functional Diversity and Specificity.Genome biology and evolution · 2024Article
- Eighteen genes primarily expressed in the testis are not required for male fertility in mice†.Biology of reproduction · 2024Article
- CRISPR/Cas9-mediated disruption of lipocalins, Ly6g5b, and Ly6g5c causes male subfertility in mice.Andrology · 2024Article
- Male Infertility: New Developments, Current Challenges, and Future Directions.The world journal of men's health · 2024Review
- Individual disruption of 12 testis-enriched genes via the CRISPR/Cas9 system does not affect the fertility of male mice.Journal of reproductive immunology · 2024Article
- A Comparative Full-Length Transcriptome Analysis Using Oxford Nanopore Technologies (ONT) in Four Tissues of Bovine Origin.Animals : an open access journal from MDPI · 2024Article
- Thirteen Ovary-Enriched Genes Are Individually Not Essential for Female Fertility in Mice.Cells · 2024Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
25 authors at 9 institutions in 4 countries.
Funding
Abstract
More than 1000 genes are predicted to be predominantly expressed in mouse testis, yet many of them remain unstudied in terms of their roles in spermatogenesis and sperm function and their essentiality in male reproduction. Since individually indispensable factors can provide important implications for the diagnosis of genetically related idiopathic male infertility and may serve as candidate targets for the development of nonhormonal male contraceptives, our laboratories continuously analyze the functions of testis-enriched genes in vivo by generating knockout mouse lines using the CRISPR/Cas9 system. The dispensability of genes in male reproduction is easily determined by examining the fecundity of knockout males. During our large-scale screening of essential factors, we knocked out 30 genes that have a strong bias of expression in the testis and are mostly conserved in mammalian species including human. Fertility tests reveal that the mutant males exhibited normal fecundity, suggesting these genes are individually dispensable for male reproduction. Since such functionally redundant genes are of diminished biological and clinical significance, we believe that it is crucial to disseminate this list of genes, along with their phenotypic information, to the scientific community to avoid unnecessary expenditure of time and research funds and duplication of efforts by other laboratories.
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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.