Related Experiment Video

Updated: Oct 17, 2025

Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
08:33

Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis

Published on: December 5, 2017

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CCRK/CDK20 regulates ciliary retrograde protein trafficking via interacting with BROMI/TBC1D32

Tatsuro Noguchi1, Kentaro Nakamura1, Yuuki Satoda1

  • 1Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto, Japan.

Plos One
|October 8, 2021
PubMed

Insights

CCRK regulates ciliary protein trafficking and cilia length by interacting with BROMI and activating ICK. This process is crucial for proper ciliary function and involves the turnaround of intraflagellar transport proteins.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cilia Biology

Background:

  • CCRK/CDK20 interacts with BROMI/TBC1D32, regulating ciliary Hedgehog signaling.
  • Mutations in CCRK and ICK/CILK1 orthologs cause cilia elongation.
  • ICK regulates retrograde ciliary protein trafficking and the turnaround of proteins at ciliary tips.

Purpose of the Study:

  • To elucidate the cooperative mechanism of CCRK and ICK in regulating ciliary protein trafficking.
  • To investigate the role of CCRK in ciliary protein trafficking and cilia length regulation.

Main Methods:

  • Phenotypic analysis of CCRK-knockout cells.
  • Rescue experiments using wild-type and mutant CCRK expression.
  • Assessment of intraflagellar transport (IFT) protein accumulation and ciliary membrane protein enrichment.

Main Results:

  • CCRK-knockout cells exhibit phenotypes similar to ICK-knockout cells, including IFT protein overaccumulation at bulged ciliary tips and enrichment of GPR161 and Smoothened.
  • Exogenous expression of wild-type CCRK rescued CCRK-knockout cell phenotypes.
  • Kinase-dead or BROMI-binding defective CCRK mutants failed to rescue the observed phenotypes.

Conclusions:

  • CCRK regulates the turnaround process at ciliary tips in conjunction with BROMI.
  • CCRK likely activates ICK to control ciliary protein trafficking and cilia length.
  • CCRK's kinase activity and BROMI interaction are essential for its function in cilia regulation.

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