Controlling contractile instabilities in the actomyosin cortex

  1. Masatoshi Nishikawa
  2. Sundar Ram Naganathan
  3. Frank Jülicher
  4. Stephan W Grill  Is a corresponding author
  1. Technical University Dresden, Germany
  2. Max Planck Institute for the Physics of Complex Systems, Germany
  3. Technische Universität, Germany

Abstract

The actomyosin cell cortex is an active contractile material for driving cell- and tissue morphogenesis. The cortex has a tendency to form a pattern of myosin foci, which is a signature of potentially unstable behavior. How a system that is prone to such instabilities can reliably drive morphogenesis remains an outstanding question. Here we report that in Caenorhabditis elegans zygote, feedback between active RhoA and myosin induces a contractile instability in the cortex. We discover that an independent RhoA pacemaking oscillator controls this instability, generating a pulsatory pattern of myosin foci and preventing the collapse of cortical material into a few dynamic contracting regions. Our work reveals how contractile instabilities that are natural to occur in mechanically active media can be biochemically controlled in order to robustly drive morphogenetic events.

Article and author information

Author details

  1. Masatoshi Nishikawa

    Biotechnology Center, Technical University Dresden, Dresden, Germany
    Competing interests
    No competing interests declared.
  2. Sundar Ram Naganathan

    Biotechnology Center, Technical University Dresden, Dresden, Germany
    Competing interests
    No competing interests declared.
  3. Frank Jülicher

    Max Planck Institute for the Physics of Complex Systems, Dresden, Germany
    Competing interests
    Frank Jülicher, Reviewing editor, eLife.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-4731-9185
  4. Stephan W Grill

    Biotechnology Center, Technische Universität, Dresden, Germany
    For correspondence
    stephan.grill@tu-dresden.de
    Competing interests
    No competing interests declared.

Funding

Deutsche Forschungsgemeinschaft (SPP 1782,GSC 97,GR 3271/2,GR 3271/3,GR 3271/4)

  • Stephan W Grill

European Research Council (281903)

  • Stephan W Grill

Human Frontier Science Program (RGP0023/2014)

  • Stephan W Grill

European Commission (ITN grant - 281903)

  • Stephan W Grill

Max-Planck-Gesellschaft

  • Stephan W Grill

European Commission (ITN grant - 641639)

  • Stephan W Grill

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Copyright

© 2017, Nishikawa et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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https://doi.org/10.7554/eLife.19595