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A more recent version of this article appeared on January 1, 2004
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Submitted on May 29, 2003
Revised on August 20, 2003
Accepted on August 28, 2003
1 Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655
2 Istituto Pasteur-Fondazione Cenci Bolognetti and Istituto di Biologia e Patologia Molecolari del CNR, Dipartimento di Genetica e Biologia Molecolare, Universita di Roma "La Sapienza", P.le Aldo Moro 5, 00185 Roma Italy
* Corresponding author. E-mail address: andrea.pereira{at}umassmed.edu.
We have performed a mutational analysis together with RNA interference to determine the role of the kinesin-like protein KLP67A in Drosophila cell division. During both mitosis and male meiosis, Klp67A mutations cause an increase in MT length and disrupt discrete aspects of spindle assembly, as well as cytokinesis. Mutant cells exhibit greatly enlarged metaphase spindle as a result of excessive MT polymerization. The analysis of both living and fixed cells also shows perturbations in centrosome separation, chromosome segregation and central spindle assembly. These data demonstrate that the MT plus end directed motor, KLP67A, is essential for spindle assembly during mitosis and male meiosis, and suggest that the regulation of MT plus end polymerization is a key determinant of spindle architecture throughout cell division.
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