Journal of Biomedical Science

, Volume 12, Issue 2, pp 297–310

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


  • Hua-Ling Chen
    • Institute of Biomedical SciencesAcademia Sinica
  • Chieh-Ju C. Tang
    • Institute of Biomedical SciencesAcademia Sinica
  • Chiung-Ya Chen
    • Institute of Biomedical SciencesAcademia Sinica
    • Institute of Biomedical SciencesAcademia Sinica

DOI: 10.1007/s11373-005-0980-0

Cite this article as:
Chen, H., Tang, C.C., Chen, C. et al. J Biomed Sci (2005) 12: 297. doi:10.1007/s11373-005-0980-0


Aurora kinases are emerging as key regulators of centrosome function, chromosome segregation and cytokinesis. We previously isolated Aurora-C (Aie1), 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 histone 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.


Aurora kinasecell cyclechromosome segregationcytokinesismeiosismitosis

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© National Science Council, Taipei 2005