Fig. 4

Fig. 4

a, b Actomyosin enrichment (magenta gradient) at the front of migrating cells promotes bleb initiation either by causing breaks within the actin cortex or by detaching the cortex from the plasma membrane. Accordingly, the region of the cell front containing a high level of actomyosin is more prone to subsequent blebbing (bleb-prone region, BPR). Myosin-dependent contractility also generates a contractile force (F_{contractility}) that results in retrograde cortical flow, together with the actomyosin-rich structure present at the cell front (Actin flow velocity v, black arrow). In wild-type cells, actin in PGCs is coupled to that in surrounding cells via E-cadherin; this coupling restricts the bleb-prone region at the leading edge by frictional forces resisting the actomyosin-driven flows (γ_wt, wild-type). Upon a depletion of E-cadherin (E-cadherin knockdown scenario), the friction opposing the actin retrograde flows (γ_KD) is lower. As a result, the bleb-prone region spreads towards the back of the cell, and blebbing events occur in a less coordinated manner. The shape of the spread can be predicted by a transport-decay model to be an exponential function, where λ is a characteristic length that depends inversely on the friction γ, and I_BG is the background fluorescence. (For more details on the mathematical modelling, see Methods). c Exponential fits of the actin fluorescence intensity in the PGCs derived from the signal profiles shown in Supplementary Fig. 4a, d upon decreasing the actin to membrane linkage by the expression of DN E-cadherin or β-catenin mutant (for the fits of e-cadherin^weg/weg mutant and e-cadherin MO see Supplementary Fig. 9). As predicted by the transport-decay model, in each case the decay length of E-cadherin knockdown (λ_KD) is larger than in the control (λ_wt) situation: λ_KD > λ_wt. This suggests that the overall actin polarity is reduced when the friction with the environment is reduced.