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The Cep57-pericentrin module organizes PCM expansion and centriole engagement

Author

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  • Koki Watanabe

    (National Institute of Genetics
    The Graduate University for Advanced Studies (SOKENDAI)
    The University of Tokyo)

  • Daisuke Takao

    (National Institute of Genetics
    The University of Tokyo)

  • Kei K Ito

    (The University of Tokyo)

  • Mikiko Takahashi

    (Teikyo Heisei University)

  • Daiju Kitagawa

    (National Institute of Genetics
    The Graduate University for Advanced Studies (SOKENDAI)
    The University of Tokyo)

Abstract

Centriole duplication occurs once per cell cycle to ensure robust formation of bipolar spindles and chromosome segregation. Each newly-formed daughter centriole remains connected to its mother centriole until late mitosis. The disengagement of the centriole pair is required for centriole duplication. However, the mechanisms underlying centriole engagement remain poorly understood. Here, we show that Cep57 is required for pericentriolar material (PCM) organization that regulates centriole engagement. Depletion of Cep57 causes PCM disorganization and precocious centriole disengagement during mitosis. The disengaged daughter centrioles acquire ectopic microtubule-organizing-center activity, which results in chromosome mis-segregation. Similar defects are observed in mosaic variegated aneuploidy syndrome patient cells with cep57 mutations. We also find that Cep57 binds to the well-conserved PACT domain of pericentrin. Microcephaly osteodysplastic primordial dwarfism disease pericentrin mutations impair the Cep57-pericentrin interaction and lead to PCM disorganization. Together, our work demonstrates that Cep57 provides a critical interface between the centriole core and PCM.

Suggested Citation

  • Koki Watanabe & Daisuke Takao & Kei K Ito & Mikiko Takahashi & Daiju Kitagawa, 2019. "The Cep57-pericentrin module organizes PCM expansion and centriole engagement," Nature Communications, Nature, vol. 10(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-08862-2
    DOI: 10.1038/s41467-019-08862-2
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    Cited by:

    1. Jung-Eun Park & Tae-Sung Kim & Yan Zeng & Melissa Mikolaj & Jong Ahn & Muhammad S. Alam & Christina M. Monnie & Victoria Shi & Ming Zhou & Tae-Wook Chun & Frank Maldarelli & Kedar Narayan & Jinwoo Ahn, 2024. "Centrosome amplification and aneuploidy driven by the HIV-1-induced Vpr•VprBP•Plk4 complex in CD4+ T cells," Nature Communications, Nature, vol. 15(1), pages 1-18, December.
    2. Yutaka Takeda & Takumi Chinen & Shunnosuke Honda & Sho Takatori & Shotaro Okuda & Shohei Yamamoto & Masamitsu Fukuyama & Koh Takeuchi & Taisuke Tomita & Shoji Hata & Daiju Kitagawa, 2024. "Molecular basis promoting centriole triplet microtubule assembly," Nature Communications, Nature, vol. 15(1), pages 1-15, December.
    3. Revati Darp & Marc A. Vittoria & Neil J. Ganem & Craig J. Ceol, 2022. "Oncogenic BRAF induces whole-genome doubling through suppression of cytokinesis," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

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