Ccdc87 is critical for sperm function and male fertility.

Biol Reprod

State Key Laboratory of Molecular Biology, Shanghai Key Laboratory of Molecular Andrology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.

Published: October 2018

AI Article Synopsis

  • Male infertility is linked to various factors, including genetics, with specific genes like Ccdc87 playing a critical role.
  • Ccdc87 is expressed only in the testis and is essential for proper sperm function; without it, male mice showed subfertility and abnormal sperm.
  • The study shows that disruption of Ccdc87 leads to reduced sperm motility, issues with acrosome reaction, and significantly lowered fertilizing capacity, highlighting its importance in male fertility.

Article Abstract

Male infertility has become an increasingly common health concern in recent years. Apart from environmental factors, nutrition, lifestyle, and sexually transmitted diseases, genetic defects are important causes of male infertility. Many genes have been demonstrated to be associated with male infertility. However, the roles of some functional genes in infertility, especially those that are specifically expressed in the reproductive system, remain to be elucidated. Here, we demonstrated that the testis-specific gene coiled-coil domain-containing 87 (Ccdc87) is critical for male fertility. Reverse-transcriptase polymerase chain reaction and western blot analyses revealed that the Ccdc87 mRNA and protein were only expressed in mouse testis. Ccdc87 expression first appeared at postnatal day 14 and remained at a relatively high level until adulthood. Male mice lacking Ccdc87 gene (Ccdc87-/-) were found to be subfertile. Approximately 20% of Ccdc87-null sperm from the testis and epididymis displayed severe abnormity of acrosome and cell nucleus. Sperm isolated from the cauda epididymides of Ccdc87-/- mice exhibited decreased initial motility but did not show any change in capacitation. Additionally, Ccdc87 disruption led to the impotency of sperm spontaneous and progesterone-induced acrosome reaction. Moreover, in vitro fertilization assays indicated that the fertilizing capacity of Ccdc87-/- sperm was significantly reduced. Taken together, these findings provide a new clue to understand the genetic causes of male infertility.

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Source
http://dx.doi.org/10.1093/biolre/ioy106DOI Listing

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