ArticleBiology of reproduction2020
The testis-specific serine proteases PRSS44, PRSS46, and PRSS54 are dispensable for male mouse fertility†.
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 31 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
31 citing papers in PubMed, 40 citations in OpenAlex.
- 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
- Multiomic Selection of Cancer-Testis Antigens as Precision Immuno-oncologic Targets in Head and Neck Cancer.JAMA otolaryngology-- head & neck surgery · 2025Article
- Molecular Evolution of theAnimals : an open access journal from MDPI · 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
- Article
- Genome-Wide Analysis ofInternational journal of molecular sciences · 2023Article
- The EGF-motif-containing protein SPE-36 is a secreted sperm protein required for fertilization in C. elegans.Current biology : CB · 2023Article
- Testis-specific serine kinase 3 is required for sperm morphogenesis and male fertility.Andrology · 2023Article
- Phenotype Compensation in Reproductive ADAM Gene Family: A Case Study with ADAM27 Knockout Mouse.Iranian journal of biotechnology · 2022Article
- Two acquired mouse Y chromosome-linked genes, Prssly and Teyorf1, are dispensable for male fertility‡.Biology of reproduction · 2022Article
- Article
- X-linked palindromic gene families 4930567H17Rik and Mageb5 are dispensable for male mouse fertility.Scientific reports · 2022Article
- TMPRSS12 Functions in Meiosis and Spermiogenesis and Is Required for Male Fertility in Mice.Frontiers in cell and developmental biology · 2022Article
- Endocrine disorders and fertility and pregnancy: An update.Frontiers in endocrinology · 2022Review
- Mutation ofFrontiers in physiology · 2022Article
- Inactivation of testis-specific gene C4orf46 is dispensable for spermatogenesis and fertility in mouse.Mammalian genome : official journal of the International Mammalian Genome Society · 2021Article
- 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
- Article
- Retinoic Acid Induced Protein 14 (PeerJ · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
High-throughput transcriptomics and proteomics approaches have recently identified a large number of germ cell-specific genes with many that remain to be studied through functional genetics approaches. Serine proteases (PRSS) constitute nearly one-third of all proteases, and, in our bioinformatics screens, we identified many that are testis specific. In this study, we chose to focus on Prss44, Prss46, and Prss54, which we confirmed as testis specific in mouse and human. Based on the analysis of developmental expression in the mouse, expression of all four genes is restricted to the late stage of spermatogenesis concomitant with a potential functional role in spermiogenesis, spermiation, or sperm function. To best understand the male reproductive requirement and functional roles of these serine proteases, each gene was individually ablated by CRISPR/Cas9-mediated ES cell or zygote approach. Homozygous deletion mutants for each gene were obtained and analyzed for phenotypic changes. Analyses of testis weights, testis and epididymis histology, sperm morphology, and fertility revealed no significant differences in Prss44, Prss46, and Prss54 knockout mice in comparison to controls. Our results thereby demonstrate that these genes are not required for normal fertility in mice, although do not preclude the possibility that these genes may function in a redundant manner. Elucidating the individual functional requirement or lack thereof of these novel genes is necessary to build a better understanding of the factors underlying spermatogenesis and sperm maturation, which has implications in understanding the etiology of male infertility and the development of male contraceptives.
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