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Description
Summary
The mechanical aspects of embryonic morphogenesis have been in most cases simulated using finite element models, which describe the tissue as a continuous medium. Here we develop a simulation of Drosophila embryo invagination of its ventral mesoderm during gastrulation, that allows access to both cellular and multicellular mechanical behaviours of the embryo. This model can be viewed as multi-agent where the individuals are the cell membranes characterized by an acto-myosin cortical tension and connected by apical and basal junctions and an acto-myosin contractile ring at the apical junctions. They interact with each other through hydrodynamic flow.
Behaviours observed in vivo, including apical junction movements at the onset of gastrulation, cell elongation and subsequent shortening during invagination, and the development of a dorso-ventral gradient of thickness of the embryo, are predicted by this model as passive mechanical consequences of the genetically and biochemically controlled increase in the apical surface tension in invaginating mesoderm cells.
In a second step, we also implemented the biochemical control system we investigated through experiments on the embryo. Here, a second set of individual agents are the cells and their gene expressions. We showed that ventral invagination initiation can be explained by a positive mechanical feedback. Under this hypothesis, the simulations account for the phenotypes observed in wild-type embryos and all the main mutants for invagination.
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Philippe-Alexandre Pouille