Each cell of an animal has the same genome. Nevertheless, those cells can express many different phenotypes, associated to different shapes and architectures. It has been recently shown that the mechanical environment can influence both cell shape and phenotype. Thus, we can wonder how a cell gets its shape and what part its mechanical environment plays in it. In general, a shape results from an equilibrium of forces beetwen the inside and the outside. In the cell, the tensile forces exerted by the acto-myosin cytoskeleton are transmitted to the substrate through proteins aggregates named adhesion complexes. Here, we studied the early spreading of fibroblasts, an event in which those cells go from a spherical shape to an isotropic spread shape. In order to determine how adhesion formation correlates with the tension released to the substrate during this process, we built up a setup able to measure the cellular traction forces in a uniaxial geometry and to monitor simultaneously the organization of adhesion complexes through TIRF microscopy. This setup permitted us to develop a scenario of cell spreading in two phases. In the first phase, the spreading is fast, the force is null and no adhesion complexe is visible. The transition to the second phase occurs when the shape of the cell body reach a critical contact angle of 90°. Here, the force starts to build up followed by adhesions and a slow-down of cell spreading. We next investigated how the mechanical environment could affect this scenario. To do that, we first modified the stiffness of our force probe; then, we compared the pattern of adhesion for a cell spreading on one plate or between two microplates.
