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Phosphorylation of EB2 by Aurora B and CDK1 ensures mitotic progression and genome stability

Author

Listed:
  • Makoto Iimori

    (Graduate School of Medical Sciences, Kyushu University)

  • Sugiko Watanabe

    (Innovative Anticancer Strategy for Therapeutics and Diagnosis Group, Innovation Center for Medical Redox Navigation, Kyushu University
    Present address: Department of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan.)

  • Shinichi Kiyonari

    (Nagoya University Graduate School of Medicine)

  • Kazuaki Matsuoka

    (Innovative Anticancer Strategy for Therapeutics and Diagnosis Group, Innovation Center for Medical Redox Navigation, Kyushu University
    Taiho Pharmaceutical Co., Ltd.)

  • Ryo Sakasai

    (Kanazawa Medical University)

  • Hiroshi Saeki

    (Graduate School of Medical Sciences, Kyushu University)

  • Eiji Oki

    (Graduate School of Medical Sciences, Kyushu University)

  • Hiroyuki Kitao

    (Graduate School of Medical Sciences, Kyushu University
    Innovative Anticancer Strategy for Therapeutics and Diagnosis Group, Innovation Center for Medical Redox Navigation, Kyushu University)

  • Yoshihiko Maehara

    (Innovative Anticancer Strategy for Therapeutics and Diagnosis Group, Innovation Center for Medical Redox Navigation, Kyushu University
    Graduate School of Medical Sciences, Kyushu University)

Abstract

Temporal regulation of microtubule dynamics is essential for proper progression of mitosis and control of microtubule plus-end tracking proteins by phosphorylation is an essential component of this regulation. Here we show that Aurora B and CDK1 phosphorylate microtubule end-binding protein 2 (EB2) at multiple sites within the amino terminus and a cluster of serine/threonine residues in the linker connecting the calponin homology and end-binding homology domains. EB2 phosphorylation, which is strictly associated with mitotic entry and progression, reduces the binding affinity of EB2 for microtubules. Expression of non-phosphorylatable EB2 induces stable kinetochore microtubule dynamics and delays formation of bipolar metaphase plates in a microtubule binding-dependent manner, and leads to aneuploidy even in unperturbed mitosis. We propose that Aurora B and CDK1 temporally regulate the binding affinity of EB2 for microtubules, thereby ensuring kinetochore microtubule dynamics, proper mitotic progression and genome stability.

Suggested Citation

  • Makoto Iimori & Sugiko Watanabe & Shinichi Kiyonari & Kazuaki Matsuoka & Ryo Sakasai & Hiroshi Saeki & Eiji Oki & Hiroyuki Kitao & Yoshihiko Maehara, 2016. "Phosphorylation of EB2 by Aurora B and CDK1 ensures mitotic progression and genome stability," Nature Communications, Nature, vol. 7(1), pages 1-14, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11117
    DOI: 10.1038/ncomms11117
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