To advance this problem, we reasoned that one way to connect molecular activities to large-scale functions is to assess phenotypic consequences of individual gene inhibitions at larger scales, and analyse these in the context of a physical theory. But we are still a long way from understanding the mechanisms by which molecular-scale activities drive large-scale events such as actomyosin-driven flows, cell division and migration. Over the last three decades, mutational and RNAi-based genetic screens have provided a catalogue of proteins that are involved in various developmental processes ( Perrimon et al., 2010 Mohr and Perrimon, 2012).
We speculate that morphogenetic degeneracies contribute to the robustness of bulk biological matter in development.Ĭell and tissue-scale morphogenetic processes are driven by well-orchestrated molecular activities and signalling pathways. This is indicative for a ‘morphogenetic degeneracy’ where multiple molecular processes contribute to the same large-scale physical property. By performing a candidate RNAi screen of ABPs and actomyosin regulators we demonstrate that perturbing distinct molecular processes can lead to similar flow phenotypes. However, which molecular activities contribute to flow dynamics and large-scale physical properties such as viscosity and active torque is largely unknown. Large-scale flow dynamics can be captured by active gel theory by considering force balances and conservation laws in the actomyosin cortex. elegans zygotes, where large-scale flows emerge from the collective action of actomyosin filaments and actin binding proteins (ABPs). We investigated this problem in the context of actomyosin-based cortical flow in C. One of the great challenges in biology is to understand the mechanisms by which morphogenetic processes arise from molecular activities.
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