Dr Nicolas Cuny

How morphological diversity arises from variations in biomechanical processes remains an open question. Although forces shape tissues, how force-generating systems differ across species to create diverse forms is unclear. Here, we combine comparative morphogenesis and active matter theory across six cnidarian species spanning 500 million years of divergence to identify the mechanical basis of larval shape diversity. We define species-specific configurations of mechanical modules-termed mechanotypes-that quantitatively predict larval shapes across taxa. We find that shape elongation is a simple trait at the mesoscale level, as its variation depends on one mechanical module, whereas shape polarity is a complex trait dependent on several modules. Perturbations mimicking interspecies regulatory differences reshape these modules, reprogramming larval morphology into forms resembling sister species. By establishing a mesoscale mechanical framework for cross-species comparison, this work reveals how variations in a limited set of tissue-scale parameters generate morphological diversity.

Blood vessels expand and contract actively as they continuously experience dynamic external stresses from blood flow. The mechanical response of the vessel wall is that of a composite material: its mechanical properties depend on its cellular components, which change dynamically as the cells respond to external stress. Mapping the relationship between these underlying cellular processes and emergent tissue mechanics is an ongoing challenge, particularly in endothelial cells. Here we assess the mechanics and cellular dynamics of an endothelial tube using a microstretcher that mimics the native environment of blood vessels. The characterization of the instantaneous monolayer elasticity reveals a strain-stiffening, actin-dependent and substrate-responsive behaviour. After a physiological pressure increase, the tissue displays a fluid-like expansion, with the reorientation of cell shape and actin fibres. We introduce a mechanical model that considers the actin fibres as a network in the nematic phase and couples their dynamics with active and elastic fibre tension. The model accurately describes the response to the pressure of endothelial tubes.

Blood vessels expand and contract actively as they continuously experience dynamic external stresses from blood flow. The mechanical response of the vessel wall is that of a composite material: its mechanical properties depend on its cellular components, which change dynamically as the cells respond to external stress. Mapping the relationship between these underlying cellular processes and emergent tissue mechanics is an ongoing challenge, particularly in endothelial cells. Here we assess the mechanics and cellular dynamics of an endothelial tube using a microstretcher that mimics the native environment of blood vessels. The characterization of the instantaneous monolayer elasticity reveals a strain-stiffening, actin-dependent and substrate-responsive behaviour. After a physiological pressure increase, the tissue displays a fluid-like expansion, with the reorientation of cell shape and actin fibres. We introduce a mechanical model that considers the actin fibres as a network in the nematic phase and couples their dynamics with active and elastic fibre tension. The model accurately describes the response to the pressure of endothelial tubes.