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Published online 12 June 2006. doi:10.1083/jcb.200511132
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 173, Number 6, 879-891
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Article

 HURP controls spindle dynamics to promote proper interkinetochore tension and efficient kinetochore capture

Jim Wong and Guowei Fang

Department of Biological Sciences, Stanford University, Stanford, CA 94305

Correspondence to Guowei Fang: gwfang{at}stanford.edu

Through a functional genomic screen for mitotic regulators, we identified hepatoma up-regulated protein (HURP) as a protein that is required for chromosome congression and alignment. In HURP-depleted cells, the persistence of unaligned chromosomes and the reduction of tension across sister kinetochores on aligned chromosomes resulted in the activation of the spindle checkpoint. Although these defects transiently delayed mitotic progression, HeLa cells initiated anaphase without resolution of these deficiencies. This bypass of the checkpoint arrest provides a tumor-specific mechanism for chromosome missegregation and genomic instability. Mechanistically, HURP colocalized with the mitotic spindle in a concentration gradient increasing toward the chromosomes. HURP binds directly to microtubules in vitro and enhances their polymerization. In vivo, HURP stabilizes mitotic microtubules, promotes microtubule polymerization and bipolar spindle formation, and decreases the turnover rate of the mitotic spindle. Thus, HURP controls spindle stability and dynamics to achieve efficient kinetochore capture at prometaphase, timely chromosome congression to the metaphase plate, and proper interkinetochore tension for anaphase initiation.

Abbreviations used in this paper: APC/C, anaphase-promoting complex/cyclosome; FLIP, fluorescence loss in photobleaching; HURP, hepatoma up-regulated protein; MAP, microtubule-associated protein; NEB, nuclear envelope breakdown.


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