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Morphogenetic degeneracies in the actomyosin cortex.

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Naganathan,  Sundar Ram
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Fürthauer,  Sebastian
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Cannistraci,  Carlo Vittorio
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Grill,  Stephan W.
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Citation

Naganathan, S. R., Fürthauer, S., Rodriguez, J., Fievet, B. T., Jülicher, F., Ahringer, J., et al. (2018). Morphogenetic degeneracies in the actomyosin cortex. eLife, 7: e37677. doi:10.7554/eLife.37677.


Cite as: https://hdl.handle.net/21.11116/0000-0003-F651-C
Abstract
One of the great challenges in biology is to understand the mechanisms by which morphogenetic processes arise from molecular activities. We investigated this problem in the context of actomyosin-based cortical flow in C. elegans zygotes, where large-scale flows emerge from the collective action of actomyosin filaments and actin binding proteins (ABPs). Large-scale flow dynamics can be captured by active gel theory by considering force balances and conservation laws in the actomyosin cortex. However, which molecular activities contribute to flow dynamics and large-scale physical properties such as viscosity and active torque is largely unknown. By performing a candidate RNAi screen of ABPs and actomyosin regulators we demonstrate that perturbing distinct molecular processes can lead to similar flow phenotypes. This is indicative for a 'morphogenetic degeneracy' where multiple molecular processes contribute to the same large-scale physical property. We speculate that morphogenetic degeneracies contribute to the robustness of bulk biological matter in development.