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

Author:
  • Ida Björkgren
  • Luis Alvarez
  • Nelli Blank
  • Melanie Balbach
  • Heikki Turunen
  • Teemu Daniel Laajala
  • Jussi Toivanen
  • Anton Krutskikh
  • Niklas Wahlberg
  • Ilpo Huhtaniemi
  • Matti Poutanen
  • Dagmar Wachten
  • Petra Sipilä
Publishing year: 2016-05-15
Language: English
Pages: 143-154
Publication/Series: Molecular and Cellular Endocrinology
Volume: 427
Document type: Journal article
Publisher: Elsevier

Abstract english

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.

Keywords

  • Zoology
  • Beta-defensin
  • Epididymis
  • Flagellar motility pattern
  • ICre knock-in
  • Sperm maturation
  • Sperm-oocyte binding

Other

Published
  • ISSN: 0303-7207
Professor Niklas Wahlberg at the unit of Biodiversity, Lund University.
E-mail: niklas [dot] wahlberg [at] biol [dot] lu [dot] se

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