Open AccessSperm dysfunction and ciliopathy
Author(s) -
Inaba Kazuo,
Mizuno Katsutoshi
Publication year - 2016
Publication title -
reproductive medicine and biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.005
H-Index - 22
eISSN - 1447-0578
pISSN - 1445-5781
DOI - 10.1007/s12522-015-0225-5
Subject(s) - ciliopathy , cilium , motile cilium , flagellum , primary ciliary dyskinesia , axoneme , biology , microbiology and biotechnology , intraflagellar transport , microtubule , sperm motility , asthenozoospermia , dynein , motility , male infertility , infertility , genetics , medicine , lung , phenotype , pregnancy , bronchiectasis , gene
Sperm motility is driven by motile cytoskeletal elements in the tail, called axonemes. The structure of axonemes consists of 9 + 2 microtubules, molecular motors (dyneins), and their regulatory structures. Axonemes are well conserved in motile cilia and flagella through eukaryotic evolution. Deficiency in the axonemal structure causes defects in sperm motility, and often leads to male infertility. It has been known since the 1970s that, in some cases, male infertility is linked with other symptoms or diseases such as Kartagener syndrome. Given that these links are mostly caused by deficiencies in the common components of cilia and flagella, they are called “immotile cilia syndrome” or “primary ciliary dyskinesia,” or more recently, “ciliopathy,” which includes deficiencies in primary and sensory cilia. Here, we review the structure of the sperm flagellum and epithelial cilia in the human body, and discuss how male fertility is linked to ciliopathy.