Cohesin protein Smc3 influences kinocilial structure and function
Fiona M Mensching1,2, Niusha Banoukh1, M Kathryn Iovine1
1Department of Biological Sciences, Lehigh University, 111 Research Drive, Bethlehem, Pennsylvania 18015, USA.
Biology Open
|November 20, 2025
Summary
Cohesin subunit Smc3 impacts kinociliary structure and function, potentially linking cohesinopathies and ciliopathies. Smc3 knockdown in zebrafish hair cells reduced kinociliary length and impaired function.
Area of Science:
- Developmental Biology
- Cell Biology
- Genetics
Background:
- Cohesinopathies and ciliopathies are congenital disorders impacting similar body systems.
- The potential link between these disorders is not well understood.
- Reduced expression of cohesin subunit Smc3 in zebrafish caused abnormal otolith development, suggesting a role in kinociliary function.
Purpose of the Study:
- To investigate the role of cohesin subunit Smc3 in kinociliary development and function.
- To explore the potential link between cohesinopathy and ciliopathy.
Main Methods:
- Utilized zebrafish posterior lateral line neuromasts and hair cells.
- Performed Smc3 knockdown and assessed kinociliary length.
- Monitored neomycin resistance and FM1-43X uptake in hair cells to evaluate kinociliary function and mechanotransduction.
Main Results:
- Smc3 knockdown led to reduced kinociliary length in hair cells.
- Posterior lateral line neuromasts exhibited neomycin resistance, indicating impaired kinocilium function.
- No defects in FM1-43X uptake were observed, but hair cell number was reduced.
Conclusions:
- Cohesin subunit Smc3 plays a significant role in ciliary structure and function.
- This study provides preliminary evidence linking cohesinopathy and ciliopathy etiologies.
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