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Vol. 15, Issue 4, 1793-1801, April 2004

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HIV-1 Vpr Induces Defects in Mitosis, Cytokinesis, Nuclear Structure, and Centrosomes

Fred Chang ^* , Fabio Re ^* , Sarah Sebastian , Shelley Sazer , and Jeremy Luban   ^||

Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, New York 10032; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York 10032; and Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas 77030

Submitted September 24, 2003; Revised December 10, 2003; Accepted December 14, 2003
Monitoring Editor: Tim Stearns

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 proteins, sad1p and the polo kinase plo1p, were delocalized in vpr-expressing yeast cells, suggesting that spindle pole body 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.

^* These authors contributed equally to this work.

^|| Corresponding author. E-mail address: jl45{at}columbia.edu.

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