ArticleAndrology2024
CRISPR/Cas9-mediated disruption of lipocalins, Ly6g5b, and Ly6g5c causes male subfertility in mice.
Article in Andrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Testis expressed 50 is essential for maintaining sperm acrosome integrity during epididymal transit.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Expression Patterns and Functional Implications of CMTM2 in Human Testis and Sperm.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Epididymis-specific RNase A family genes regulate fertility and small RNA processing.The Journal of biological chemistry · 2024Article
- Epididymis-specific RNase A family genes regulate fertility and small RNA processing.bioRxiv : the preprint server for biology · 2024Article
- Unlocking Genetic Mysteries during the Epic Sperm Journey toward Fertilization: Further ExpandingBiomolecules · 2024Review
- Distinct actions of testicular endocrine and lumicrine signaling on the proximal epididymal transcriptome.Reproductive biology and endocrinology : RB&E · 2024Article
- CUB domains are not required for OVCH2 function in sperm maturation in the mouse epididymis.Andrology · 2024Article
- Expression of NELL2/NICOL-ROS1 lumicrine signaling-related molecules in the human male reproductive tract.Reproductive biology and endocrinology : RB&E · 2024Article
- Comprehensive time-course gene expression evaluation of high-risk beef cattle to establish immunological characteristics associated with undifferentiated bovine respiratory disease.Frontiers in immunology · 2024Article
- Lumicrine signaling: Extracellular regulation of sperm maturation in the male reproductive tract lumen.Genes to cells : devoted to molecular & cellular mechanisms · 2023Review
- Transcriptome profiling of the initial segment and proximal caput of mouse epididymis.Frontiers in endocrinology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSpermatozoa become mature and competent for fertilization during transit from the caput epididymis to the cauda epididymis. However, detailed molecular mechanisms of epididymal sperm maturation are still unclear. Here, we focused on multiple epididymis-enriched genes: lipocalin family genes (Lcn5, Lcn6, Lcn8, Lcn9, and Lcn10) and Ly6 family genes (Ly6g5b and Ly6g5c). These genes are evolutionarily conserved in mammals and form clusters on chromosomes 2 and 17 in the mouse, respectively.
objectiveTo clarify whether these genes are required for epididymal sperm maturation and acquisition of fertilizing ability, we generated knockout (KO) mice using the CRISPR/Cas9 system and analyzed their phenotype. MATERIALS AND
methodsWe generated four lines of KO mice: Lcn9 single KO, the lipocalin family quadruple KO (Lcn5, Lcn6, Lcn8, and Lcn10), quintuple KO (Lcn5, Lcn6, Lcn8, Lcn10, and Lcn9), and double KO of Ly6 family genes (Ly6g5b and Ly6g5c).
resultsAlthough the Lcn9 single KO did not affect male fertility, the quadruple KO and quintuple KO male mice were subfertile and mostly infertile, respectively, with a reduced amount of ADAM3, an essential protein for sperm binding to the zona pellucida. Further analysis revealed that the quintuple KO spermatozoa lack the CMTM2A/B that are required for ADAM3 maturation. Intriguingly, Ly6g5b and Ly6g5c double KO male mice also showed subfertility with reduced sperm ADAM3.
conclusionThese results suggest epididymal secretory proteins are involved in ADAM3 maturation and acquisition of sperm fertilizing ability.
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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.