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Mitotic centromere-associated kinesin is important for anaphase chromosome segregation
T Maney1, A W Hunter, M Wagenbach
1Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, Washington 98195, USA.
Abstract:
Mitotic centromere-associated kinesin (MCAK) is recruited to the centromere at prophase and remains centromere associated until after telophase. MCAK is a homodimer that is encoded by a single gene and has no associated subunits. A motorless version of MCAK that binds centromeres but not microtubules disrupts chromosome segregation during anaphase. Antisense-induced depletion of MCAK results in the same defect. MCAK overexpression induces centromere-independent bundling and eventual loss of spindle microtubule polymer suggesting that centromere-associated bundling and/or depolymerization activity is required for anaphase. Live cell imaging indicates that MCAK may be required to coordinate the onset of sister centromere separation.
Insights
Mitotic centromere-associated kinesin (MCAK) is crucial for proper chromosome segregation. Depleting or altering MCAK function disrupts cell division, highlighting its role in coordinating centromere separation.
Area of Science:
- Cell Biology
- Molecular Biology
- Genetics
Background:
- Mitotic centromere-associated kinesin (MCAK) is a key motor protein involved in cell division.
- MCAK localizes to centromeres from prophase through telophase.
- It functions as a homodimer without associated subunits.
Purpose of the Study:
- To investigate the role of MCAK in chromosome segregation and microtubule dynamics during mitosis.
- To determine the consequences of MCAK motor function disruption and depletion on cell division.
Main Methods:
- Utilizing a motorless MCAK mutant to assess binding and functional effects.
- Employing antisense-induced depletion to reduce MCAK levels.
- Overexpression of MCAK to observe effects on microtubule polymerization.
- Live cell imaging to monitor chromosome and spindle dynamics.
Main Results:
- A motorless MCAK mutant that binds centromeres but not microtubules impairs chromosome segregation.
- Antisense-induced depletion of MCAK leads to similar chromosome segregation defects.
- MCAK overexpression causes microtubule bundling and loss, independent of centromere binding.
- Live cell imaging suggests MCAK coordinates the initiation of sister centromere separation.
Conclusions:
- MCAK's centromere-associated microtubule depolymerization activity is essential for accurate anaphase progression.
- MCAK plays a critical role in regulating spindle dynamics and ensuring timely sister centromere separation.