Aurora-C kinase supports mitotic progression in the absence of Aurora-B

Scott D. Slattery, Michael A. Mancini, Bill R. Brinkley, Rebecca M. Hall

Research output: Contribution to journalArticle

58 Scopus citations

Abstract

Aurora family kinases regulate numerous mitotic processes, and their dysfunction or overexpression can cause aneuploidy, a contributing factor for tumorigenesis. In vertebrates, the Aurora-B kinase regulates kinetochore maturation, destabilization of improper kinetochore-microtubule attachments, the spindle assembly checkpoint, central spindle organization and cytokinesis. A gene duplication event created the related Aurora-C kinase in mammals. While Aurora-C function is unclear, it has similar structural and localization properties as Aurora-B. Inhibition of either Aurora-B or Aurora-C function causes aneuploidy, while simultaneous inhibition of both causes a higher frequency of aneuploidy. to determine if Aurora-C and -B have overlapping or unique complementary functions during mitosis, we created a system where Aurora-B is replaced by wild-type or kinase-defective mutant Aurora-C in HeLa cells. In this model, Aurora-B protein levels and mitotic functions were suppressed including the regulation of kinetochore-microtubule attachments, the spindle assembly checkpoint, and cytokinesis. Wild-type, but not kinase-defective Aurora-C expression, was able to rescue these functions. therefore, Aurora-C can perform the same essential functions as Aurora-B in mitosis.

Original languageEnglish
Pages (from-to)2986-2997
Number of pages12
JournalCell Cycle
Volume8
Issue number18
DOIs
StatePublished - Sep 15 2009

Keywords

  • Aurora-B
  • Aurora-C
  • Chromosome congression
  • High content analysis
  • High throughput microscopy
  • Mitosis
  • Spindle assembly checkpoint

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

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