PUBLICATION
            Calaxin is a key factor for calcium-dependent waveform control in zebrafish sperm
- Authors
 - Morikawa, M., Yamaguchi, H., Kikkawa, M.
 - ID
 - ZDB-PUB-240615-15
 - Date
 - 2024
 - Source
 - Life science alliance 7(9): (Journal)
 - Registered Authors
 - Kikkawa, Masahide
 - Keywords
 - none
 - MeSH Terms
 - 
    
        
        
            
                
- Zebrafish Proteins*/genetics
 - Zebrafish Proteins*/metabolism
 - Zebrafish*
 - Animals, Genetically Modified*
 - Dyneins*/genetics
 - Dyneins*/metabolism
 - Calcium*/metabolism
 - Cilia/metabolism
 - Animals
 - Male
 - Spermatozoa*/metabolism
 - Spermatozoa*/physiology
 - Flagella/metabolism
 - Flagella/physiology
 - Calcium-Binding Proteins/genetics
 - Calcium-Binding Proteins/metabolism
 - Sperm Motility/genetics
 - Sperm Motility/physiology
 
 - PubMed
 - 38876797 Full text @ Life Sci Alliance
 
            Citation
        
        
            Morikawa, M., Yamaguchi, H., Kikkawa, M. (2024) Calaxin is a key factor for calcium-dependent waveform control in zebrafish sperm. Life science alliance. 7(9):.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                Calcium is critical for regulating the waveform of motile cilia and flagella. Calaxin is currently the only known molecule involved in the calcium-dependent regulation in ascidians. We have recently shown that Calaxin stabilizes outer arm dynein (OAD), and the knockout of Calaxin results in primary ciliary dyskinesia phenotypes in vertebrates. However, from the knockout experiments, it was not clear which functions depend on calcium and how Calaxin regulates the waveform. To address this question, here, we generated transgenic zebrafish expressing a mutant E130A-Calaxin deficient in calcium binding. E130A-Calaxin restored the OAD reduction of calaxin-/- sperm and the abnormal movement of calaxin-/- left-right organizer cilia, showing that Calaxin's stabilization of OADs is calcium-independent. In contrast, our quantitative analysis of E130A-Calaxin sperms showed that the calcium-induced asymmetric beating was not restored, linking Calaxin's calcium-binding ability with an asymmetric flagellar beating for the first time. Our data show that Calaxin is a calcium-dependent regulator of the ciliary beating and a calcium-independent OAD stabilizer.
            
    
        
        
    
    
    
                
                    
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