Targeted inactivation of the mouse epididymal beta-defensin 41 alters sperm flagellar beat pattern and zona pellucida binding
Research output: Contribution to journal › Article
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 Defb41iCre/iCre knock-in mice lacked Defb41 expression and displayed iCre recombinase activity in the principal cells of the proximal epididymis. Heterozygous Defb41iCre/+ mice can be used to generate epididymis specific conditional knock-out mouse models. Homozygous Defb41iCre/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 Defb41iCre/iCre sperm and weaker binding to the oocyte. Thus, DEFB41 is required for proper sperm maturation.
|Research areas and keywords||
Subject classification (UKÄ) – MANDATORY
|Number of pages||12|
|Journal||Molecular and Cellular Endocrinology|
|Publication status||Published - 2016 May 15|