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Published online November 26, 2007
doi:10.1083/jcb.200707120
The Journal of Cell Biology, Vol. 179, No. 5, 869-879
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Wordeman et al.
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Article

 MCAK facilitates chromosome movement by promoting kinetochore microtubule turnover

Linda Wordeman1, Michael Wagenbach1, and George von Dassow2

1 Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, WA 98195
2 Center for Cell Dynamics, University of Washington Friday Harbor Laboratories, Friday Harbor, WA 98250

Correspondence to Linda Wordeman: worde{at}u.washington.edu

Mitotic centromere-associated kinesin (MCAK)/Kif2C is the most potent microtubule (MT)-destabilizing enzyme identified thus far. However, MCAK's function at the centromere has remained mechanistically elusive because of interference from cytoplasmic MCAK's global regulation of MT dynamics. In this study, we present MCAK chimeras and mutants designed to target centromere-associated MCAK for mechanistic analysis. Live imaging reveals that depletion of centromere-associated MCAK considerably decreases the directional coordination between sister kinetochores. Sister centromere directional antagonism results in decreased movement speed and increased tension. Sister centromeres appear unable to detach from kinetochore MTs efficiently in response to directional switching cues during oscillatory movement. These effects are reversed by anchoring ectopic MCAK to the centromere. We propose that MCAK increases the turnover of kinetochore MTs at all centromeres to coordinate directional switching between sister centromeres and facilitate smooth translocation. This may contribute to error correction during chromosome segregation either directly via slow MT turnover or indirectly by mechanical release of MTs during facilitated movement.

Abbreviations used in this paper: CENP, centromere protein; MCAK, mitotic centromere-associated kinesin; mRFP, monomeric RFP; MT, microtubule.


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