ArticleAndrology2019
Nine genes abundantly expressed in the epididymis are not essential for male fecundity in mice.
Article in Andrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 46 citations in OpenAlex.
- The absence of both RIBC1 and RIBC2 induces decreased sperm motility and litter size in male mice.Andrology · 2026Article
- 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
- Eighteen genes primarily expressed in the testis are not required for male fertility in mice†.Biology of reproduction · 2024Article
- USF2 and TFEB compete in regulating lysosomal and autophagy genes.Nature communications · 2024Article
- Transcriptomic Characterization of Male Formosan Pangolin (Animals : an open access journal from MDPI · 2024Article
- CRISPR/Cas9-mediated disruption of lipocalins, Ly6g5b, and Ly6g5c causes male subfertility in mice.Andrology · 2024Article
- Multiple genes in the Pate5-13 genomic region contribute to ADAM3 processing†.Biology of reproduction · 2024Article
- Busulfan administration replicated the characteristics of the epididymal initial segment observed in mice lacking testis-epididymis lumicrine signaling.The Journal of reproduction and development · 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
- Lumicrine signaling: Extracellular regulation of sperm maturation in the male reproductive tract lumen.Genes to cells : devoted to molecular & cellular mechanisms · 2023Review
- The testis-, epididymis-, or seminal vesicle-enriched genes Aldoart2, Serpina16, Aoc1l3, and Pate14 are not essential for male fertility in mice.Experimental animals · 2023Article
- The EGF-motif-containing protein SPE-36 is a secreted sperm protein required for fertilization in C. elegans.Current biology : CB · 2023Article
- Various gene modification techniques to discover molecular targets for nonhormonal male contraceptives: A review.International journal of reproductive biomedicine · 2023Review
- Transcriptome profiling of the initial segment and proximal caput of mouse epididymis.Frontiers in endocrinology · 2023Article
- Two acquired mouse Y chromosome-linked genes, Prssly and Teyorf1, are dispensable for male fertility‡.Biology of reproduction · 2022Article
- Loss of mouse Y chromosome gene Zfy1 and Zfy2 leads to spermatogenesis impairment, sperm defects, and infertility.Biology of reproduction · 2022Article
- CTRP11 contributes modestly to systemic metabolism and energy balance.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Contraceptive and Infertility Target DataBase: a contraceptive drug development tool for targeting and analysis of human reproductive specific tissues†.Biology of reproduction · 2021Article
- Y/X-Chromosome-Bearing Sperm Shows Elevated Ratio in the Left but Not the Right Testes in Healthy Mice.Life (Basel, Switzerland) · 2021Article
- FAM71F1 binds to RAB2A and RAB2B and is essential for acrosome formation and male fertility in mice.Development (Cambridge, England) · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundSpermatozoa become competent for fertilization during transit through the epididymis. As spermatozoa from the proximal caudal epididymis can fertilize eggs, proteins from the caput and corpus epididymis are required for sperm maturation.
objectivesMicroarray analysis identified that more than 17,000 genes are expressed in the epididymis; however, few of these genes demonstrate expression restricted to the epididymis. To analyze epididymis-enriched gene function in vivo, we generated knockout (KO) mutations in nine genes that are abundantly expressed in the caput and corpus region of the epididymis. MATERIALS AND
methodsKO mice were generated using the CRISPR/Cas9 system. The histology of the epididymis was observed with hematoxylin and eosin staining. KO males were caged with wild-type females for 3-6 months to check fertility.
resultsWe generated individual mutant mouse lines having indel mutations in Pate1, Pate2, or Pate3. We also deleted the coding regions of Clpsl2, Epp13, and Rnase13, independently. Finally, the 150 kb region encoding Gm1110, Glb1l2, and Glb1l3 was deleted to generate a triple KO mouse line. Histology of the epididymis and sperm morphology of all KO lines were comparable to control males. The females mated with these KO males delivered pups at comparable numbers as control males. DISCUSSION AND
conclusionWe revealed that nine genes abundantly expressed in the caput and corpus epididymis are dispensable for sperm function and male fecundity. CRISPR/Cas9-mediated KO mice generation accelerates the screening of epididymis-enriched genes for potential functions in reproduction.
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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.