KAWANO NATSUKO
   Department   Undergraduate School  , School of Agriculture
   Position   Associate Professor
Language English
Publication Date 2019
Type Academic Journal
Peer Review Peer reviewed
Title Calaxin is required for cilia-driven determination of vertebrate laterality.
Contribution Type Co-authored (other than first author)
Journal Communications biology
Journal TypeAnother Country
Volume, Issue, Page 2,pp.226
Author and coauthor Sasaki Keita, Shiba Kogiku, Nakamura Akihiro, Kawano Natsuko, Satouh Yuhkoh, Yamaguchi Hiroshi, Morikawa Motohiro, Shibata Daisuke, Yanase Ryuji, Jokura Kei, Nomura Mami, Miyado Mami, Takada Shuji, Ueno Hironori, Nonaka Shigenori, Baba Tadashi, Ikawa Masahito, Kikkawa Masahide, Miyado Kenji, Inaba Kazuo
Details Calaxin is a Ca2+-binding dynein-associated protein that regulates flagellar and ciliary movement. In ascidians, calaxin plays essential roles in chemotaxis of sperm. However, nothing has been known for the function of calaxin in vertebrates. Here we show that the mice with a null mutation in Efcab1, which encodes calaxin, display typical phenotypes of primary ciliary dyskinesia, including hydrocephalus, situs inversus, and abnormal motility of trachea cilia and sperm flagella. Strikingly, both males and females are viable and fertile, indicating that calaxin is not essential for fertilization in mice. The 9 + 2 axonemal structures of epithelial multicilia and sperm flagella are normal, but the formation of 9 + 0 nodal cilia is significantly disrupted. Knockout of calaxin in zebrafish also causes situs inversus due to the irregular ciliary beating of Kupffer's vesicle cilia, although the 9 + 2 axonemal structure appears to remain normal.
DOI 10.1038/s42003-019-0462-y
ISSN 2399-3642
PMID 31240264