Fig. 6. Reconstitution of BCL6 expression and RhoA inhibition each cause phenotypic reversion of ventral surface adhesion structures and repolarization. (A-D) A BCL6 expression construct was retrovirally transduced into Bcl6^–/– BMM and the cells sorted for GFP expression 36 hours post-infection. GFP-positive cells were plated on fibronectin-coated coverslips for 24 hours before fixation and staining for Y118 paxillin (C) and visualization of GFP expression (B). (D) Quantification of polarization indices for Bcl6^+/+, Bcl6^–/– BMM and BCL6-reconstituted Bcl6^–/– BMM (error bars, s.e.m.; *P<0.02 significantly different from index in Bcl6^+/+ BMM cells). (E-J) Bcl6^+/+ and Bcl6^–/– BMM were treated with either TBS buffer (control, E,F), Tat-tagged C3 transferase (G,H) or the ROCK1 inhibitor, Y27632 (I,J) before fixation and staining for Y118 paxillin. Treatment with another ROCK1 inhibitor, HA 1077, produced similar results to Y27632 treatment (not shown). Bar, 10 µm.