Enteropathogenic E. coli relies on collaboration between the formin mDia1 and the Arp2/3 complex for actin pedestal biogenesis and maintenance
Fig 3
An siRNA screen reveals that targeting mDia1 inhibits actin pedestal formation by EPEC.
(A) HeLa cells were treated with siRNA pairs to the indicated targets, infected with EPEC for 4 h, fixed, and stained with antibodies to detect HA-Tir (magenta) and with phalloidin to visualize F-actin (green). Scale bar, 10 µm. (B-C) The % of adherent, Tir-positive EPEC (B) or KC12+EspFU (C) that were associated with pedestals was quantified from experiments performed in A. Each bar shows the mean % +/- SEM of pedestal-forming bacteria, while black data points represent mean %s from each infected cell that harbored 10–50 bacteria (n = 15–53 cells). * p < 0.05, *** p<0.001 (ANOVA, Dunnett’s multiple comparison test). Significance asterisks in B and C are in reference to the control.