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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.
Highlights
Cell and tissue-scale morphogenetic processes are driven by well-orchestrated molecular activities and signalling pathways
Given that large-scale RNAi screens performed in C. elegans 1-cell embryos have failed to identify many of these actin binding proteins (ABPs) (Sonnichsen et al, 2005), we show that a rigorous quantification is required to identify subtle yet significant deviations from wild type cortical flow
We combined RNAi screening with phenotypic characterization in terms of hydrodynamic theory
Summary
Cell and tissue-scale morphogenetic processes are driven by well-orchestrated molecular activities and signalling pathways. We are still a long way from understanding the mechanisms by which molecular-scale activities drive large-scale events such as actomyosindriven flows, cell division and migration 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. 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 This would allow us to investigate which effective material properties are changed by which molecular perturbation, an important step forward that allows understanding of developmental processes across scales.
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