Figure 7.

Mutations in N-WASP– and SNX9-binding regions of EspF attenuate CR-induced junction disruption in vivo. (A) WT CR induced robust actin-dense pedestal formation in WT, but not iNWKO mice. (B) WT mice infected with WT CR (black line), but not CR complemented with N-WASP– or SNX9-binding–defective EspF (red and blue lines, respectively), showed weight loss during acute infection. (C) Bacterial colonization by WT CR, CRΔespF/pEspF_NWBD and CRΔespF/pEspF_SNX9BD. (D) CR expressing wild-type EspF induced marked disruption of normal ZO-1 patterns by 7 days after infection (upper right); in contrast, CRΔespF strains complemented with N-WASP or SNX9-binding–defective EspF failed to disrupt localization of ZO-1 at intercellular junctions. (E) Loss of EspF binding to host N-WASP (CRΔespF/pEspF_NWBD) attenuates increases in intestinal permeability to FITC-dextran induced by CR during in vivo infection. Scale bars: 20 μm. RLU, relative light unit.