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PKCɛ switches Aurora B specificity to exit the abscission checkpoint

Author

Listed:
  • Tanya Pike

    (Protein Phosphorylation Laboratory, The Francis Crick Institute)

  • Nicola Brownlow

    (Protein Phosphorylation Laboratory, The Francis Crick Institute
    Present address: Centre for Genomic Regulation (CRG), Dr Aiguader, 88, PRBB Building, 08003 Barcelona, Spain)

  • Svend Kjaer

    (Protein Purification Facility, Francis Crick Institute)

  • Jeremy Carlton

    (Division of Cancer Studies King’s College London)

  • Peter J. Parker

    (Protein Phosphorylation Laboratory, The Francis Crick Institute
    Division of Cancer Studies King’s College London)

Abstract

The ‘NoCut’, or Aurora B abscission checkpoint can be activated if DNA is retained in the cleavage furrow after completion of anaphase. Checkpoint failure leads to incomplete abscission and a binucleate outcome. These phenotypes are also observed after loss of PKCɛ in transformed cell models. Here we show that PKCɛ directly modulates the Aurora B-dependent abscission checkpoint by phosphorylating Aurora B at S227. This phosphorylation invokes a switch in Aurora B specificity, with increased phosphorylation of a subset of target substrates, including the CPC subunit Borealin. This switch is essential for abscission checkpoint exit. Preventing the phosphorylation of Borealin leads to abscission failure, as does expression of a non-phosphorylatable Aurora B S227A mutant. Further, depletion of the ESCRT-III component and Aurora B substrate CHMP4C enables abscission, bypassing the PKCɛ–Aurora B exit pathway. Thus, we demonstrate that PKCɛ signals through Aurora B to exit the abscission checkpoint and complete cell division.

Suggested Citation

  • Tanya Pike & Nicola Brownlow & Svend Kjaer & Jeremy Carlton & Peter J. Parker, 2016. "PKCɛ switches Aurora B specificity to exit the abscission checkpoint," Nature Communications, Nature, vol. 7(1), pages 1-10, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13853
    DOI: 10.1038/ncomms13853
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