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

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Alvarez,  Luis
Department of Molecular Sensory Systems, Center of Advanced European Studies and Research (caesar), Max Planck Society;

Blank,  Neli
Max Planck Research Group Molecular Physiology, Center of Advanced European Studies and Research (caesar), Max Planck Society;

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Balbach,  Melanie
Max Planck Research Group Molecular Physiology, Center of Advanced European Studies and Research (caesar), Max Planck Society;

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Wachten,  Dagmar
Max Planck Research Group Molecular Physiology, Center of Advanced European Studies and Research (caesar), Max Planck Society;

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Zitation

Björkgren, I., Alvarez, L., Blank, N., Balbach, M., Turunen, H., Laajala, T. D., et al. (2016). Targeted inactivation of the mouse epididymal beta-defensin 41 alters sperm flagellar beat pattern and zona pellucida binding. Molecular and Cellular Endocrinology, 427, 143-154. doi:10.1016/j.mce.2016.03.013.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-002A-15DA-E
Zusammenfassung
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.