Max Planck Institute for the Physics of Complex Systems, Dresden, Germany; Center for Computational Biology, Flatiron Institute, New York, United States
Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle, United Kingdom; Wellcome Trust/Cancer Research UK Gurdon Institute, Cambridge, United Kingdom
Bruno Thomas Fievet
Wellcome Trust/Cancer Research UK Gurdon Institute, Cambridge, United Kingdom
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.