ArticleProceedings of the National Academy of Sciences of the United States of America2016
Genome engineering uncovers 54 evolutionarily conserved and testis-enriched genes that are not required for male fertility in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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104 citing papers in PubMed, 168 citations in OpenAlex.
- The Cilia-Associated Protein CCDC89 Is Dispensable for Male Fertility in Mice.Cytoskeleton (Hoboken, N.J.) · 2026Article
- N-myristoyltransferase 1, a key gene for protein N-myristoylation, is dispensable for fertility in male mice.The Journal of reproduction and development · 2026Article
- C2orf74 orchestrates germ-Leydig crosstalk to inhibit white adipose tissue browning in male mice.Nature communications · 2026Article
- Normal spermatogenesis and fertility inBiochemistry and biophysics reports · 2026Article
- Article
- Functional analysis of genes enriched in male reproductive organs: validation via fertility assessment of 14 knockout mouse lines.Frontiers in cell and developmental biology · 2026Article
- TKTL1: a new candidate gene in non-obstructive azoospermia.Reproductive biomedicine online · 2025Article
- L-2-hydroxyglutarate regulates centromere and heterochromatin conformation in the male germline.PLoS genetics · 2025Article
- Acrosomal Matrix Proteins sp56 and AM67 and Gamete Adhesion in Mammals.Academia biology · 2025Article
- Article
- Recurrent Independent Pseudogenization Events of the Sperm Fertilization Gene ZP3r in Apes and Monkeys.Journal of molecular evolution · 2024Article
- Eighteen genes primarily expressed in the testis are not required for male fertility in mice†.Biology of reproduction · 2024Article
- 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
- Thirteen Ovary-Enriched Genes Are Individually Not Essential for Female Fertility in Mice.Cells · 2024Article
- Ovine conceptuses express phospholipase inhibitory genes on days 14-15 of pregnancy, interacting with IFNT pathways.Reproduction (Cambridge, England) · 2024Article
- Gene-deficient mouse model established by CRISPR/Cas9 system reveals 15 reproductive organ-enriched genes dispensable for male fertility.Frontiers in cell and developmental biology · 2024Article
- Adeno-associated-virus-mediated delivery of CRISPR-CasRx induces efficient RNA knockdown in the mouse testis.Theranostics · 2024Article
- Deletion ofFrontiers in cell and developmental biology · 2024Article
- The EGF-motif-containing protein SPE-36 is a secreted sperm protein required for fertilization in C. elegans.Current biology : CB · 2023Article
- Testis-specific proteins, TSNAXIP1 and 1700010I14RIK, are important for sperm motility and male fertility in mice.Andrology · 2023Article
44 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors at 3 institutions in 4 countries.
Funding
Abstract
Gene-expression analysis studies from Schultz et al. estimate that more than 2,300 genes in the mouse genome are expressed predominantly in the male germ line. As of their 2003 publication [Schultz N, Hamra FK, Garbers DL (2003) Proc Natl Acad Sci USA 100(21):12201-12206], the functions of the majority of these testis-enriched genes during spermatogenesis and fertilization were largely unknown. Since the study by Schultz et al., functional analysis of hundreds of reproductive-tract-enriched genes have been performed, but there remain many testis-enriched genes for which their relevance to reproduction remain unexplored or unreported. Historically, a gene knockout is the "gold standard" to determine whether a gene's function is essential in vivo. Although knockout mice without apparent phenotypes are rarely published, these knockout mouse lines and their phenotypic information need to be shared to prevent redundant experiments. Herein, we used bioinformatic and experimental approaches to uncover mouse testis-enriched genes that are evolutionarily conserved in humans. We then used gene-disruption approaches, including Knockout Mouse Project resources (targeting vectors and mice) and CRISPR/Cas9, to mutate and quickly analyze the fertility of these mutant mice. We discovered that 54 mutant mouse lines were fertile. Thus, despite evolutionary conservation of these genes in vertebrates and in some cases in all eukaryotes, our results indicate that these genes are not individually essential for male mouse fertility. Our phenotypic data are highly relevant in this fiscally tight funding period and postgenomic age when large numbers of genomes are being analyzed for disease association, and will prevent unnecessary expenditures and duplications of effort by others.
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