Related Experiment Video
Updated: Jun 9, 2026
05:35
Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins
Published on: March 3, 2016
MCAK/Kif2C centromeric activity level tunes K-fiber turnover through distinct pathways
Mike Wagenbach1, Juan Jesus Vicente1, Linda Wordeman1
1Department of Neurobiology and Biophysics, University of Washington School of Medicine, Seattle, WA, USA.
Iscience
|June 8, 2026
Summary
Both too little and too much MCAK/Kif2C cause chromosome segregation errors by affecting microtubule stability. This suggests a critical role for proper MCAK/Kif2C levels in ensuring accurate cell division.
Area of Science:
- Cell Biology
- Molecular Biology
- Genetics
Background:
- MCAK/Kif2C is a kinesin crucial for correcting chromosome attachment errors during cell division.
- Both depletion and overexpression of MCAK/Kif2C lead to chromosome missegregation.
- Elevated acetylated tubulin suggests altered microtubule stability in both conditions.
Purpose of the Study:
- To investigate the mechanism by which MCAK/Kif2C levels influence chromosome segregation.
- To determine the role of microtubule stability in MCAK/Kif2C-mediated errors.
Main Methods:
- Analysis of chromosome congression and missegregation.
- Measurement of acetylated tubulin levels.
- Assessment of microtubule-kinetochore interactions.
Main Results:
- Reduced MCAK/Kif2C increased lateral microtubule interactions due to altered tubulin ratios.
- Overexpressed MCAK/Kif2C stabilized end-on microtubule interactions, increasing kinetochore-microtubule interactions and k-fiber stability.
- Both extremes of MCAK/Kif2C levels resulted in increased chromosome segregation errors.
Conclusions:
- MCAK/Kif2C levels critically regulate microtubule dynamics at kinetochores.
- Aberrant MCAK/Kif2C levels promote chromosome missegregation through altered k-fiber stability.
- Maintaining optimal MCAK/Kif2C concentration is essential for accurate chromosome segregation.
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