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A more recent version of this article appeared on December 1, 2007
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Submitted on February 15, 2007
Revised on August 24, 2007
Accepted on September 6, 2007
*Cambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 2XY, United Kingdom;
Medical Research Council Laboratory of Molecular Biology, Cambridge CB2 2QH, United Kingdom
Monitoring Editor: Erika Holzbaur
Myosin VI plays important roles in endocytic and exocytic membrane trafficking pathways in cells. Because recent work has highlighted the importance of targeted membrane transport during cytokinesis, we investigated whether myosin VI plays a role in this process during cell division. In dividing cells myosin VI undergoes dramatic changes in localization: in prophase myosin VI is recruited to the spindle poles and in cytokinesis myosin VI is targeted to the walls of the ingressing cleavage furrow with a dramatic concentration in the midbody region. Furthermore, myosin VI is present on vesicles moving into and out of the cytoplasmic bridge connecting the two daughter cells. Inhibition of myosin VI activity by siRNA mediated knock down or by overexpression of dominant negative myosin VI tail leads to a delay in metaphase progression and a defect in cytokinesis. GIPC, a myosin VI binding partner, is associated with myosin VIs function(s) in dividing cells. Loss of GIPC in siRNA knock down cells results in a more than fourfold increase in the number of multinucleated cells. Our results suggest that myosin VI has novel functions in mitosis and plays an essential role in targeted membrane transport during cytokinesis.
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