Controlling contractile instabilities in the actomyosin cortex
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.
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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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