IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v3y2012i1d10.1038_ncomms2062.html
   My bibliography  Save this article

Greatwall kinase and cyclin B-Cdk1 are both critical constituents of M-phase-promoting factor

Author

Listed:
  • Masatoshi Hara

    (Laboratory of Cell and Developmental Biology, Graduate School of Bioscience, Tokyo Institute of Technology
    Present address: Whitehead Institute and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA;)

  • Yusuke Abe

    (Laboratory of Cell and Developmental Biology, Graduate School of Bioscience, Tokyo Institute of Technology
    Present address: Department of Experimental Pathology, Cancer Institute of the Japanese Foundation for Cancer Research, Tokyo 135-8550, Japan;)

  • Toshiaki Tanaka

    (Laboratory of Cell Biology, Graduate School of Bioscience, Tokyo Institute of Technology)

  • Takayoshi Yamamoto

    (Laboratory of Cell and Developmental Biology, Graduate School of Bioscience, Tokyo Institute of Technology
    Present address: Department of Biological Sciences, Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan.)

  • Eiichi Okumura

    (Laboratory of Cell and Developmental Biology, Graduate School of Bioscience, Tokyo Institute of Technology)

  • Takeo Kishimoto

    (Laboratory of Cell and Developmental Biology, Graduate School of Bioscience, Tokyo Institute of Technology)

Abstract

Maturation/M-phase-promoting factor is the universal inducer of M-phase in eukaryotic cells. It is currently accepted that M-phase-promoting factor is identical to the kinase cyclin B–Cdk1. Here we show that cyclin B–Cdk1 and M-phase-promoting factor are not in fact synonymous. Instead, M-phase-promoting factor contains at least two essential components: cyclin B–Cdk1 and another kinase, Greatwall kinase. In the absence of Greatwall kinase, the M-phase-promoting factor is undetectable in oocyte cytoplasm even though cyclin B–Cdk1 is fully active, whereas M-phase-promoting factor activity is restored when Greatwall kinase is added back. Although the excess amount of cyclin B–Cdk1 alone, but not Greatwall kinase alone, can induce nuclear envelope breakdown, spindle assembly is abortive. Addition of Greatwall kinase greatly reduces the amount of cyclin B–Cdk1 required for nuclear envelope breakdown, resulting in formation of the spindle with aligned chromosomes. M-phase-promoting factor is thus a system consisting of one kinase (cyclin B–Cdk1) that directs mitotic entry and a second kinase (Greatwall kinase) that suppresses the protein phosphatase 2A-B55 which opposes cyclin B–Cdk1.

Suggested Citation

  • Masatoshi Hara & Yusuke Abe & Toshiaki Tanaka & Takayoshi Yamamoto & Eiichi Okumura & Takeo Kishimoto, 2012. "Greatwall kinase and cyclin B-Cdk1 are both critical constituents of M-phase-promoting factor," Nature Communications, Nature, vol. 3(1), pages 1-9, January.
    • Handle: RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms2062
    DOI: 10.1038/ncomms2062
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms2062
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms2062?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Luca Cardelli & Rosa D Hernansaiz-Ballesteros & Neil Dalchau & Attila Csikász-Nagy, 2017. "Efficient Switches in Biology and Computer Science," PLOS Computational Biology, Public Library of Science, vol. 13(1), pages 1-16, January.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms2062. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.