Morphogenetic degeneracies in the actomyosin cortex.
Fievet, Bruno Thomas
Grill, Stephan W
eLife Sciences Publications, Ltd
MetadataShow full item record
Naganathan, S. R., Fürthauer, S., Rodriguez, J., Fievet, B. T., Jülicher, F., Ahringer, J., Cannistraci, C. V., & et al. (2018). Morphogenetic degeneracies in the actomyosin cortex.. Elife, 7 https://doi.org/10.7554/eLife.37677
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.
Embryo, Nonmammalian, Animals, Caenorhabditis elegans, Microfilament Proteins, Actins, Myosins, Actomyosin, Caenorhabditis elegans Proteins, Rheology, RNA Interference, Morphogenesis, Fluorescence, Models, Biological, Hydrodynamics
Wellcome Trust (084598/Z/07/Z)
Wellcome Trust (101863/Z/13/Z)
European Commission Horizon 2020 (H2020) Marie Sk?odowska-Curie actions (641639)
External DOI: https://doi.org/10.7554/eLife.37677
This record's URL: https://www.repository.cam.ac.uk/handle/1810/286526
Attribution 4.0 International
Licence URL: https://creativecommons.org/licenses/by/4.0/