Abstract
Male infertility might be caused by genetic and/or environmental factors that impair spermatogenesis and epididymal sperm maturation. Here we report that heterozygous deletion of the nuclear receptor coactivator-5 (Ncoa5) gene resulted in decreased motility and progression of spermatozoa in the cauda epididymis, leading to infertility in male mice. Light microscopic and ultrastructural analysis revealed morphological defects in the spermatozoa collected from the cauda epididymis of Ncoa5+/− mice. Immunohistochemistry showed that interleukin-6 (IL-6) expression in epithelial cells of Ncoa5+/− epididymis was higher than wild type counterparts. Furthermore, heterozygous deletion of Il-6 gene in Ncoa5+/− male mice partially improved spermatozoa motility and moderately rescued infertility phenotype. Our results uncover a previously unknown physiological role of NCOA5 in the regulation of epididymal sperm maturation and suggest that NCOA5 deficiency could cause male infertility through increased IL-6 expression in epididymis.
Highlights
Male fertility counts on effective production of mature spermatozoa that is capable of fertilizing the egg
According to the data in the Human Protein Atlas, Nuclear receptor co-activator 5 (NCOA5) is expressed in seminiferous ducts and Leydig cells in testis, as well as in epithelial cells in the epididymis
We found that the protein levels of NCOA5 in nuclear receptor coactivator-5 (Ncoa5)+/− testis were decreased (Fig. S1A,B)
Summary
Male fertility counts on effective production of mature spermatozoa that is capable of fertilizing the egg. Sperm are morphologically complete but immotile and unable to carry out oocyte fertilization[4] It is only after the transit through the epididymis that the spermatozoon acquires its fertilization ability[5], by undergoing a discrete series of post-gonadal differentiation stages controlled by the surrounding epididymal environment. Such extracellular control of gamete differentiation is called epididymal sperm maturation[6]. We aimed to determine whether heterozygous deletion of Ncoa[5] affects sperm development and whether IL-6 expression mediates the effect of NCOA5 on fertility of male mice
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