Targeted inactivation of the mouse epididymal beta-defensin 41 alters sperm flagellar beat pattern and zona pellucida binding

: Bjorkgren I, Alvarez L, Blank N, Balbach M, Turunen H, Laajala TD, Toivanen J, Krutskikh A, Wahlberg N, Huhtaniemi I, Poutanen M, Wachten D, Sipila P

Publisher: ELSEVIER IRELAND LTD

: 2016

: Molecular and Cellular Endocrinology

: MOLECULAR AND CELLULAR ENDOCRINOLOGY

: MOL CELL ENDOCRINOL

: 427

: C

: 143

: 154

: 12

: 0303-7207

DOI: https://doi.org/10.1016/j.mce.2016.03.013

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/liCre) sperm and weaker binding to the oocyte. Thus, DEFB41 is required for proper sperm maturation. (C) 2016 Elsevier Ireland Ltd. All rights reserved.