ArticleBiology of reproduction2020
Prss55 but not Prss51 is required for male fertility in mice†.
Article in Biology of reproduction, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- PRSS38 Is a Novel Sperm Serine Protease Involved in Human and Mouse Fertilization.International journal of molecular sciences · 2025Article
- Rescue of male infertility by human PRSS55 in transgenic mice establishes a contraceptive research model.Scientific reports · 2025Article
- Identification of reproductive performance in Bali-polled bulls using computer-assisted semen analysis and plasma seminal proteomics.Veterinary world · 2025Article
- Large-scale CRISPR/Cas9 deletions within the WFDC gene cluster uncover gene functionality and critical roles in mammalian reproduction.Proceedings of the National Academy of Sciences of the United States of America · 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
- Molecular dissection and testing of PRSS37 function through LC-MS/MS and the generation of a PRSS37 humanized mouse model.Scientific reports · 2023Article
- Cocktails of NSAIDs and 17α Ethinylestradiol at Environmentally Relevant Doses in Drinking Water Alter Puberty Onset in Mice Intergenerationally.International journal of molecular sciences · 2023Article
- Paralogous Genes Involved in Embryonic Development: Lessons from the Eye and Other Tissues.Genes · 2022Review
- Two acquired mouse Y chromosome-linked genes, Prssly and Teyorf1, are dispensable for male fertility‡.Biology of reproduction · 2022Article
- Article
- Application of CRISPR/Cas Technology in Spermatogenesis Research and Male Infertility Treatment.Genes · 2022Review
- CEP128 is involved in spermatogenesis in humans and mice.Nature communications · 2022Article
- Proteolysis in Reproduction: Lessons From Gene-Modified Organism Studies.Frontiers in endocrinology · 2022Review
- Mutation ofFrontiers in physiology · 2022Article
- TMPRSS12 Functions in Meiosis and Spermiogenesis and Is Required for Male Fertility in Mice.Frontiers in cell and developmental biology · 2022Article
- Testis-expressed protein 33 is not essential for spermiogenesis and fertility in mice.Molecular medicine reports · 2021Article
- PRSS55 plays an important role in the structural differentiation and energy metabolism of sperm and is required for male fertility in mice.Journal of cellular and molecular medicine · 2021Article
- Discovery of potent thrombin inhibitors from a protease-focused DNA-encoded chemical library.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Mammalian spermatozoa are produced in the testis through spermatogenesis and matured in the epididymis to acquire fertilizing ability. Spermatozoa are ejaculated and migrate from the uterus to the oviducts to fuse with oocytes. Although over 2000 genes are expressed abundantly in mouse testes, the genes responsible for male fertility are not yet fully clarified. Here, we focused on two testis-enriched serine protease genes, Serine protease (Prss) 51 and Prss55, which overlap their gene loci partially in both mice and humans. To characterize their functions in male fertility, we first generated Prss51 and Prss55 double knockout (DKO) mice by CRISPR/Cas9 system and found that the DKO mice were sterile. DKO spermatozoa exhibit impaired migration from the uterus to the oviduct and impaired ability to bind the zona pellucida (ZP) of oocytes. Moreover, a sperm membrane protein, ADAM3 (a disintegrin and metalloprotease 3), which plays a role in sperm migration through uterotubal junction (UTJ) and sperm-ZP binding, disappeared in the DKO spermatozoa from the epididymis. We next generated single knockout (KO) mice lacking Prss51 and found that Prss51 KO mice are fertile. We also generated single KO mice lacking Prss55 and found that Prss55 KO mice phenocopy the DKO mice, demonstrating impaired sperm migration and sperm-ZP binding and a severe defect in fertility. We conclude that Prss55, but not Prss51, is required for male fertility in mice, by stabilizing ADAM3 protein for efficient sperm-UTJ migration and sperm-ZP binding. Our findings have implications for understanding additional genetic causes of the idiopathic male infertility and for the development of male or female contraceptives.
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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.