|
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 Type | Another 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 |