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. 2015 Jan 5;208(1):23–32. doi: 10.1083/jcb.201409108

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© 2015 Daneshjou et al.

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Figure 5. — Inhibition of actomyosin tension at AJs reduces the rate of VE-cadherin dissociation. (A) Cells expressing VE-t and treated with cRO. FRET/CFP ratio was determined within the control (−UV; 1) and cRO uncaging (+UV; 2) zones, shown enlarged in B. VE-cad, VE-cadherin. (B) Spatial increase in FRET/CFP ratio after cRO uncaging within irradiation zone (2) and not the adjacent zone (1). Ratio images were scaled from 0 to 5. (C) Changes in FRET ratio for VE-t with and without cRO uncaging; means ± SD, n = 8–11; *, P < 0.05; **, P < 0.005. (D) Time-lapse images of VE-cadherin–Dendra2 before and after photoconversion within the irradiation zone (circles) in cells untreated (top; basal) or treated with cRO (middle) after uncaging or blebbistatin (bottom; +Blb). (E) VE-cadherin dissociation rate was calculated as in Fig. 2 D; means ± SEM, n = 6–12. a.u., arbitrary unit. (F) Rate constant of VE-cadherin dissociation calculated from E for basal (0.23 ± 0.07min⁻¹), cRO uncaging (0.13 ± 0.05 min⁻¹), and blebbistatin (0.13 ± 0.02 min⁻¹); means ± SD, n = 8–11 cells; *, P < 0.05; ***, P < 0.0005. (G) Working model of Rac1-mediated stabilization of VE-cadherin adhesion. Rac1 relieves actomyosin tension across the adhesion, by inhibiting RhoA–ROCK-mediated signaling, leading to increased affinity for VE-cadherin trans-interaction and decreased VE-cadherin dissociation from AJs. Times are given in minutes and seconds. Bars, 10 µm.