HIV-1 Vpr induces defects in mitosis, cytokinesis, nuclear structure, and centrosomes

被引:42
作者
Chang, F
Re, FB
Sebastian, S
Sazer, S
Luban, J
机构
[1] Columbia Univ Coll Phys & Surg, Dept Microbiol, New York, NY 10032 USA
[2] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA
[3] Baylor Coll Med, Dept Biochem & Mol Biol, Houston, TX 77030 USA
关键词
D O I
10.1091/mbc.E03-09-0691
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:1793 / 1801
页数:9
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