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KDM3A coordinates actin dynamics with intraflagellar transport to regulate cilia stability
Patricia L Yeyati1, Rachel Schiller2, Girish Mali3
1Medical Research Council Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU Scotland, UK patricia.yeyati@igmm.ed.ac.uk pleasantine.mill@igmm.ed.ac.uk.
The Journal of Cell Biology
|March 2, 2017
Summary
The histone lysine demethylase KDM3A negatively regulates ciliogenesis by controlling actin dynamics. Its absence leads to abnormal cilia length and intraflagellar transport (IFT) protein accumulation.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Cilia assembly and disassembly are intrinsically linked to actin dynamics for cellular responses.
- The histone lysine demethylase KDM3A is crucial for homeostasis, with its dysfunction linked to ciliopathies and cancer prognosis.
Purpose of the Study:
- To elucidate the role of KDM3A in integrating cilia dynamics with actin regulation.
- To understand how KDM3A modulates intraflagellar transport (IFT) protein recruitment during ciliogenesis.
Main Methods:
- Utilized KDM3A loss-of-function mouse models to study ciliary defects.
- Investigated the interplay between KDM3A, actin cytoskeleton, and IFT proteins.
- Manipulated actin filament formation and depolymerization to assess rescue effects.
Main Results:
- KDM3A absence promotes ciliogenesis but results in aberrant axonemal lengths and delayed disassembly.
- KDM3A regulates actin gene expression and directly binds the actin cytoskeleton, forming an 'actin gate' involving ARP2/3 and IFT.
- Restoring actin filament formation rescued KDM3A mutant ciliary defects, while actin depolymerization mimicked these defects.
Conclusions:
- KDM3A acts as a negative regulator of ciliogenesis.
- KDM3A is essential for controlled IFT protein recruitment via actin dynamics modulation.
- KDM3A's dual role in actin regulation is critical for proper cilia function and disassembly.
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