Fig. 4. A minimal theoretical description of the cortex captures the role of contractility in thickness fluctuations.

(A) Illustration of the physical description of the cortex introducing the polymerization from the surface and the active stresses in the directions tangential (σ_xx) and perpendicular (σ_yy) to the membrane. (B) Snapshot of a numerical simulation using the cortex theoretical description illustrated in (A). The cortex locally deforms into protruding peaks because of the stress anisotropies in the actomyosin material. (C) Temporal evolution of the cortex thickness at one arbitrary spatial coordinate from a simulation at low contractile activity (a = 7, red) and at a higher contractile activity (a = 7.75, blue). The time unit is defined as the inverse of the gel’s disassembly rate k (see Materials and Methods). (D) Representation of the cortex median thickness and fluctuation amplitude from experiments on control cells (i), CK666-treated cells (ii), and blebbistatin-treated cells (iii). Cells are sorted in ascending value of the median thickness (square). The length of the vertical line between the thickness first decile (upward triangle) and last decile (downward triangle) represents the fluctuation amplitude. The thickness fluctuations appear larger for larger cortex thicknesses for control cells but not for blebbistatin-treated cells. (E) Slopes from linear regression of fluctuation amplitudes as a function of cortex thickness from the experiments for control cells (blue) and cells treated with SMIFH2 (green, overlapping control), CK666 (light purple), blebbistatin (yellow), and LatA (dark purple). The colored area of each curve represents half the 95% confidence interval. The correlation of fluctuation amplitude with cortex thickness is markedly stronger for control and nucleator inhibition compared to myosin II inhibition. (F) Slopes for the theoretical relation between thickness and fluctuation amplitude calculated from simulations at varying activity (dots). a.u., arbitrary units.