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A more recent version of this article appeared on October 1, 2006
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Submitted on July 5, 2006
Revised on August 2, 2006
Accepted on August 4, 2006
*Instituto de Biologia Molecular e Celular, Universidade do Porto, 4150-180 Porto, Portugal; Department of Cell Biology and Genetics, Erasmus Medical Centre, 3000 DR Rotterdam, The Netherlands; Division of Molecular Medicine, New York State Department of Health, Wadsworth Center, Albany, NY 12201; ¶Wellcome Trust Centre for Cell Biology, Institute of Cell and Molecular Biology, University of Edinburgh, EH9 3JR Edinburgh, United Kingdom; ||Laboratory of Cell and Molecular Biology, Faculdade de Medicina, Universidade do Porto, 4200-319 Porto, Portugal
Monitoring Editor: Kerry Bloom
CLASPs are widely conserved microtubule plus-end-tracking proteins with essential roles in the local regulation of microtubule dynamics. In yeast, Drosophila and Xenopus a single CLASP orthologue is present, which is required for mitotic spindle assembly by regulating microtubule dynamics at the kinetochore. In mammals, however, only CLASP1 has been directly implicated in cell division, despite the existence of a second paralogue, CLASP2, whose mitotic roles remain unknown. Here we show that CLASP2 localization at kinetochores, centrosomes and spindle throughout mitosis is remarkably similar to CLASP1, both showing fast microtubule-independent turnover rates. Strikingly, primary fibroblasts from Clasp2 knockout mice show numerous spindle and chromosome segregation defects that can be partially rescued by ectopic expression of Clasp1 or Clasp2. Moreover, chromosome segregation rates during anaphase A and B are slower in Clasp2 knockout cells, which is consistent with a role of CLASP2 in the regulation of kinetochore and spindle function. Noteworthy, cell viability/proliferation and spindle checkpoint function were not impaired in Clasp2 knockout cells, but the fidelity of mitosis was strongly compromised leading to severe chromosomal instability in adult cells. Together, our data support that the partially redundancy of CLASPs during mitosis acts as a possible mechanism to prevent aneuploidy in mammals.
These authors contributed equally to this work.
Address correspondence to:
Helder Maiato (maiato{at}ibmc.up.pt)
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