Extended Data Fig. 6: Activity and tension drive hole formation.
From: Mechanical stress driven by rigidity sensing governs epithelial stability
(a) Inhibition of arp2/3 by 100 µM CK666 treatment prevents hole formation on 2.3 kPa gels. Scale bar, 100 µm. Upper panel represents control, and lower panel represents CK666 treated monolayer at 0 h and 16 h. Three independent experiments were performed with same results. (b) Number of holes/mm2 under control, CK666 and blebbistatin (5 µM) treated samples averaged over n = 33 for control, n = 24 for CK666 and n = 23 for blebbistatin (two-tailed unpaired t-test, ****Pctrl_CK666 = 0.00000039, *Pctrl_bbn = 0.04). Solid lines represent mean and error bars represent standard deviation. (c) Area of holes formed under control (n = 49) and 5 µM blebbistatin treated (n = 14) samples (n.s. = non-significant). (d) Averaged velocity profile around +1/2 defects with CK666 treatment (left) (nCK666 = 2294) and WT (right) (nWT = 2646) monolayers on soft (2.3 kPa) gels. Solid lines represent mean and error bars represent standard deviation. (e) Simulations with a lower active stress (left; n = 4750 defects) as compared to the control case (right; n = 8553 defects, soft gel set of parameters, SupplementaryTable 1 SI). Colour bars refer to the magnitude of the average velocity field. Black arrows represent the direction of the average velocity vectors. White symbols represent the centre and orientation of the +1/2 defect.
