IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v8y2017i1d10.1038_s41467-017-00977-8.html
   My bibliography  Save this article

Actomyosin polarisation through PLC-PKC triggers symmetry breaking of the mouse embryo

Author

Listed:
  • Meng Zhu

    (Department of Physiology, Development and Neuroscience, University of Cambridge)

  • Chuen Yan Leung

    (Department of Physiology, Development and Neuroscience, University of Cambridge)

  • Marta N. Shahbazi

    (Department of Physiology, Development and Neuroscience, University of Cambridge)

  • Magdalena Zernicka-Goetz

    (Department of Physiology, Development and Neuroscience, University of Cambridge)

Abstract

Establishment of cell polarity in the mammalian embryo is fundamental for the first cell fate decision that sets aside progenitor cells for both the new organism and the placenta. Yet the sequence of events and molecular mechanism that trigger this process remain unknown. Here, we show that de novo polarisation of the mouse embryo occurs in two distinct phases at the 8-cell stage. In the first phase, an apical actomyosin network is formed. This is a pre-requisite for the second phase, in which the Par complex localises to the apical domain, excluding actomyosin and forming a mature apical cap. Using a variety of approaches, we also show that phospholipase C-mediated PIP2 hydrolysis is necessary and sufficient to trigger the polarisation of actomyosin through the Rho-mediated recruitment of myosin II to the apical cortex. Together, these results reveal the molecular framework that triggers de novo polarisation of the mouse embryo.

Suggested Citation

  • Meng Zhu & Chuen Yan Leung & Marta N. Shahbazi & Magdalena Zernicka-Goetz, 2017. "Actomyosin polarisation through PLC-PKC triggers symmetry breaking of the mouse embryo," Nature Communications, Nature, vol. 8(1), pages 1-16, December.
  • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00977-8
    DOI: 10.1038/s41467-017-00977-8
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-017-00977-8
    File Function: Abstract
    Download Restriction: no

    File URL: https://libkey.io/10.1038/s41467-017-00977-8?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
    ---><---

    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:8:y:2017:i:1:d:10.1038_s41467-017-00977-8. 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.