Fig. 5: F-actin architecture determines force generation, transmission, and membrane deformations.

a A phase diagram of the maximum membrane strain and the maximum actin polarity for different F-actin cortex architectures. The data points with error bars represent mean ± SD (In mixed, n = 33 liposomes and N = 2 independent experiments in [mDia1]/[Arp2/3] = 0; n = 28 and N = 2 in 1/25; n = 26 and N = 2 in 1/5; n = 41 and N = 2 in 1/2; n = 32 and N = 3 in 1; n = 23 and N = 2 in 5; n = 36 and N = 2 in 25. In mDia1 only, n = 31 and N = 2 in [mDia1]=25 nM; n = 36 and N = 2 in 125 nM; n = 49 and N = 2 in 625 nM. In 3 × [Arp2/3], n = 31 and N = 3 in [mDia1]=0 nM; n = 22 and N = 2 in 25 nM; n = 29 and N = 3 in 125 nM). b Schematic represents the F-actin architectural control of membrane deformations shown in (a). c Schematic summarizing the F-actin architectural control of force generation, transmission, and membrane deformations. The Arp2/3-nucleated cortex branches the F-actin network and forms membrane-to-cortex links, which provide a no-slip boundary-like condition. However, the contractility is attenuated within the highly branched actin gel. In contrast, the mDia1-nucleated cortex allows force generation within the network, while the unbranched nature of the network results in the slip boundary-like condition without membrane deformation. When both the Arp2/3-nucleated branch and mDia1-nucleated linear filaments coexist, contractility within the F-actin network is transmitted to the adjacent membrane, inducing a significant membrane deformation.