カワノ　ナツコ   KAWANO NATSUKO   河野　菜摘子    所属   明治大学  農学部    職種   専任准教授
言語種別	英語
発行・発表の年月	2019
形態種別	学術雑誌
査読	査読あり
標題	Calaxin is required for cilia-driven determination of vertebrate laterality.
執筆形態	共著(筆頭者以外)
掲載誌名	Communications biology
掲載区分	国外
巻・号・頁	2,pp.226
著者・共著者	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
概要	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