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. 2010 Sep 7;78(11):4532–4541. doi: 10.1128/IAI.00802-10

FIG. 1.

FIG. 1.

InlB-mediated entry of Listeria requires the host GAP ARAP2. (A) Effect of siRNA molecules on ARAP2 expression. HeLa cells were left untreated (−) or transfected with a control siRNA or either of two siRNA molecules targeting ARAP2 (ARAP2-1 or ARAP2-2). At about 48 h posttransfection, cells were solubilized for measurement of ARAP2 expression by Western blotting. (B) Effect of siRNAs targeting ARAP2 on entry or association of Listeria. Transfected HeLa cells were infected with wild-type (Wt) Listeria or an isogenic mutant strain with inlB deleted (ΔinlB). Panel i, bacterial entry was assessed using a gentamicin protection assay (37). Panel ii, association of bacteria with host cells was measured as described previously (8). Values are averages ± standard errors of the means (SEM) from three or four experiments. *, P < 0.01 compared to the no-siRNA control (−). **, P < 0.001. (C) Effect of ARAP2 depletion on internalization of Listeria, as determined by a fluorescence microscopy-based assay (38). Values are averages ± standard deviations (SD) from three experiments. *, P < 0.01 compared to control siRNA conditions. **, P < 0.001.