Controlling contractile instabilities in the actomyosin cortex
- Technical University Dresden, Germany
- Max Planck Institute for the Physics of Complex Systems, Germany
- 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
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.
Metrics
-
- 4,586
- views
-
- 1,063
- downloads
-
- 90
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
A two-part list of links to download the article, or parts of the article, in various formats.
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
Controlling contractile instabilities in the actomyosin cortex
eLife 6:e19595.
https://doi.org/10.7554/eLife.19595
Further reading
-
- Physics of Living Systems
Vertebrates have evolved great diversity in the number of segments dividing the trunk body, however, the developmental origin of the evolvability of this trait is poorly understood. The number of segments is thought to be determined in embryogenesis as a product of morphogenesis of the pre-somitic mesoderm (PSM) and the periodicity of a molecular oscillator active within the PSM known as the segmentation clock. Here, we explore whether the clock and PSM morphogenesis exhibit developmental modularity, as independent evolution of these two processes may explain the high evolvability of segment number. Using a computational model of the clock and PSM parameterised for zebrafish, we find that the clock is broadly robust to variation in morphogenetic processes such as cell ingression, motility, compaction, and cell division. We show that this robustness is in part determined by the length of the PSM and the strength of phase coupling in the clock. As previous studies report no changes to morphogenesis upon perturbing the clock, we suggest that the clock and morphogenesis of the PSM exhibit developmental modularity.
