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Updated: May 24, 2025
05:35
Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins
Published on: March 3, 2016
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MCAK/Kif2C centromeric activity level tunes K-fiber stability
Linda Wordeman1, Mike Wagenbach1, Juan Jesus Vicente1
1Department of Neurobiology and Biophysics, University of Washington School of Medicine, Seattle, WA, USA.
Biorxiv : the Preprint Server for Biology
|March 3, 2025
Summary
Correcting chromosome attachment errors requires optimal levels of the MCAK/Kif2C protein. Both too little and too much MCAK/Kif2C at centromeres increase chromosome mis-segregation by affecting microtubule stability.
Area of Science:
- Cell Biology
- Molecular Biology
- Genetics
Background:
- The kinesin MCAK/Kif2C is crucial for correcting chromosome attachment errors during cell division.
- Imbalances in MCAK/Kif2C levels at kinetochores lead to mitotic defects.
Purpose of the Study:
- To investigate the role of MCAK/Kif2C concentration at centromeres in chromosome segregation.
- To determine the mechanism by which MCAK/Kif2C concentration affects k-fiber stability and congression.
Main Methods:
- Studied cells with depleted or overexpressed MCAK/Kif2C.
- Measured inter-kinetochore distances (IKDs) and acetylated tubulin levels.
- Assessed the conversion of lateral to end-on kinetochore-microtubule attachments.
Main Results:
- Both MCAK/Kif2C depletion and overexpression resulted in delayed chromosome congression and increased mis-segregation.
- Elevated centromeric MCAK/Kif2C levels increased inter-kinetochore distances and k-fiber stability.
- Loss of MCAK/Kif2C delayed the transition from lateral to end-on kinetochore motility.
Conclusions:
- Optimal centromeric MCAK/Kif2C levels are essential for proper chromosome segregation.
- MCAK/Kif2C regulates k-fiber stability, and deviations from optimal levels impair chromosome attachment and movement.
- Centromeric MCAK/Kif2C activity is key for timely k-fiber turnover and congression during mitosis.
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