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A more recent version of this article appeared on April 1, 2004
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Submitted on September 24, 2003
Revised on December 10, 2003
Accepted on December 14, 2003
1 Department of Microbiology, Columbia University College of Physicians and Surgeons, 701 West 168th St., New York, NY 10032
2 Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030
3 Departments of Microbiology and Medicine, Columbia University College of Physicians and Surgeons, 701 West 168th St., New York, NY 10032
* Corresponding author. E-mail address: jl45{at}columbia.edu.
Human immunodeficiency virus type 1 (HIV-1) Vpr is a 15 kDa accessory protein that contributes to several steps in the viral replication cycle and promotes virus-associated pathology. Previous studies demonstrated that Vpr inhibits G2/M cell cycle progression in both human cells and in the fission yeast Schizosaccharomyces pombe. Here we report that, upon induction of vpr expression, fission yeast exhibited numerous defects in the assembly and function of the mitotic spindle. In particular, two spindle pole body (SPB) proteins, sad1p and the polo kinase plo1p, were delocalized in vpr-expressing yeast cells, suggesting that SPB integrity was perturbed. In addition, nuclear envelope structure, contractile actin ring formation and cytokinesis were also disrupted. Similar Vpr-induced defects in mitosis and cytokinesis were observed in human cells, including aberrant mitotic spindles, multiple centrosomes, and multinucleate cells. These defects in cell division and centrosomes might account for some of the pathological effects associated with HIV-1 infection.
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