Related Experiment Video
Updated: Sep 27, 2026
Analysis of Epididymal Protein Synthesis and Secretion
Published on: August 25, 2018
Targeted inactivation of the mouse epididymal beta-defensin 41 alters sperm flagellar beat pattern and zona pellucida
Ida Björkgren1, Luis Alvarez2, Nelli Blank3
1Department of Physiology and Turku Center for Disease Modeling, Institute of Biomedicine, University of Turku, Turku, Finland; Turku Doctoral Programme of Biomedical Sciences, Turku, Finland.
Abstract:
During epididymal maturation, sperm acquire the ability to swim progressively by interacting with proteins secreted by the epididymal epithelium. Beta-defensin proteins, expressed in the epididymis, continue to regulate sperm motility during capacitation and hyperactivation in the female reproductive tract. We characterized the mouse beta-defensin 41 (DEFB41), by generating a mouse model with iCre recombinase inserted into the first exon of the gene. The homozygous Defb41(iCre/iCre) knock-in mice lacked Defb41 expression and displayed iCre recombinase activity in the principal cells of the proximal epididymis. Heterozygous Defb41(iCre/+) mice can be used to generate epididymis specific conditional knock-out mouse models. Homozygous Defb41(iCre/iCre) sperm displayed a defect in sperm motility with the flagella primarily bending in the pro-hook conformation while capacitated wild-type sperm more often displayed the anti-hook conformation. This led to a reduced straight line motility of Defb41(iCre/iCre) sperm and weaker binding to the oocyte. Thus, DEFB41 is required for proper sperm maturation.
Insights
Beta-defensin 41 (DEFB41) is crucial for sperm motility and maturation. Mice lacking DEFB41 showed impaired sperm swimming and oocyte binding, highlighting its essential role in male fertility.
Area of Science:
- Reproductive Biology
- Molecular Genetics
- Sperm Physiology
Background:
- Sperm gain progressive motility during epididymal maturation via epithelial secretions.
- Beta-defensins (DEFB) regulate sperm motility during capacitation and hyperactivation.
Purpose of the Study:
- To characterize the role of mouse beta-defensin 41 (DEFB41) in sperm maturation.
- To generate a mouse model for studying DEFB41 function in the epididymis.
Main Methods:
- Generated Defb41(iCre/iCre) knock-in mice lacking DEFB41 expression.
- Assessed iCre recombinase activity in epididymal principal cells.
- Analyzed sperm motility and flagellar bending in wild-type and Defb41 deficient sperm.
- Evaluated sperm-oocyte binding efficiency.
Main Results:
- Defb41(iCre/iCre) mice showed no DEFB41 expression and had iCre activity in proximal epididymal principal cells.
- Homozygous Defb41(iCre/iCre) sperm exhibited defective motility, with flagella predominantly in a pro-hook conformation.
- Capacitated wild-type sperm displayed an anti-hook conformation more frequently.
- Defb41 deficient sperm showed reduced straight-line motility and weaker oocyte binding.
Conclusions:
- DEFB41 is essential for normal sperm maturation and motility.
- The study provides a valuable mouse model for investigating epididymis-specific gene functions.
- DEFB41 plays a critical role in sperm's ability to bind to the oocyte.
