|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | |||||
| ||||||||||||||||||||
Files in this Data Supplement:
Fig. S1. Rac1-dependent destabilization of cadherin adhesion does not require myosin contractility. (a) Keratinocytes were injected with active Rac1 (Rac1Q61L) in the presence or absence of the ROCK inhibitor Y27632. After a 6-hour incubation, cells were fixed and stained for Myc and E-cadherin. (b) Active Rac1 (Rac1Q61L) and ROCK kinase-dead mutant (ROCK kd) were microinjected alone or in combination. After 6 hours, cells were fixed and stained for Myc, FLAG-tag and α-catenin. Arrow and arrowheads indicate absence and presence of junctions, respectively. Scale bars, 16µm. (c) Quantification of the results from a and b were performed as described in Fig.3 legend (see Materials and Methods). Two different time points for expression of ROCK-kinase-dead are shown with similar results.
Fig. S2. JNK1 and CrkII signalling pathways do not cooperate with Rac1 to induce E-cadherin destabilization. Myc-tagged Rac1Q61L cDNA was injected alone with, (a) FLAG-tagged JNK1 dominant-negative mutant, JNK1(APF) or (b) with FLAG-tagged CrkII mutants cDNAs. Six hours post-injection, cells were fixed and immunostained for α-catenin, Myc and FLAG epitopes. Scale bars, 20 µm. (c) Quantification of results from a and b. The length of cadherin staining and cell-cell contact (corner to corner) for each junction were calculated and expressed as a ratio (see Materials and Methods). Differences were not statistically significant.
| ||||||||||||||||||||