AI Article Synopsis
- Calaxin is a protein that helps control the movement of cilia and flagella, and its function in sperm chemotaxis is known in ascidians, but its role in vertebrates was previously unclear.
- Mice lacking calaxin show symptoms of primary ciliary dyskinesia, such as hydrocephalus and abnormal ciliary movement, but both male and female mice remain viable and can reproduce.
- Zebrafish with calaxin knocked out exhibit irregular ciliary beating in their Kupffer's vesicle, leading to similar issues, although their axonemal structures appear normal.
Article Abstract
Calaxin is a Ca-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 , which encodes calaxin, display typical phenotypes of primary ciliary dyskinesia, including hydrocephalus, , 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 due to the irregular ciliary beating of Kupffer's vesicle cilia, although the 9 + 2 axonemal structure appears to remain normal.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6586612 | PMC |
| http://dx.doi.org/10.1038/s42003-019-0462-y | DOI Listing |
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