Overexpression of an Aurora-C kinase-deficient mutant disrupts the Aurora-B/INCENP complex and induces polyploidy

被引：43
|
作者：
Chen, HL [1 ]
Tang, CJC [1 ]
Chen, CY [1 ]
Tang, TK [1 ]
机构：
[1] Acad Sinica, Inst Biomed Sci, Taipei 11529, Taiwan
来源：
JOURNAL OF BIOMEDICAL SCIENCE | 2005年 / 12卷 / 02期
关键词：
Aurora kinase; cell cycle; chromosome segregation; cytokinesis; meiosis; mitosis;
D O I：
10.1007/s11373-005-0980-0
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Aurora kinases are emerging as key regulators of centrosome function, chromosome segregation and cytokinesis. We previously isolated Aurora-C (Aiel), a third type of Aurora kinase, in a screen for kinases expressed in mouse sperm and eggs. Currently, we know very little about the precise localization and function of Aurora-C. Immunofluorescence analysis of ectopically expressed GFP-Aurora-C has revealed that Aurora-C is a new member of the chromosomal passenger proteins localizing first to the centromeres and then to the central spindles during cytokinesis. In order to study the potential role of Aurora-C, we examined the effects of a kinase-deficient (KD) mutant (AurC-KD) in HeLa Tet-Off cells under tetracycline control. Our results showed that overexpression of AurC-KD causes defects in cell division and induces polyploidy and apoptosis. Interestingly, AurC-KD overexpression also inhibits centromere/kinetochore localization of Aurora-B, Bub1, and BubR1, reduces historic H3 phosphorylation, and disrupts the association of INCENP with Aurora-B. Together, our results showed that Aurora-C is a chromosomal passenger protein, which may serve as a key regulator in cell division.
引用
收藏
页码：297 / 310
页数：14
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