Skip to main content
. Author manuscript; available in PMC: 2017 Aug 10.
Published in final edited form as: Cell Host Microbe. 2016 Jul 21;20(2):226–237. doi: 10.1016/j.chom.2016.06.010

Figure 6. Fucosylation is required for T3SS2 effector translocation and translocon insertion but not bacterial adhesion.

Figure 6

(A) Adhesion of T3SS− V. parahemolyticus to HT-29 cells alone or treated with 50mM 2-FF or to SLC35C1 mutant cells. The T3SS− Δmam7 ΔmshA1 ΔvpadF strain was included as a negative control. (B) Survival kinetics of HT-29 and SLC35C1 mutant cells infected with T3SS2+ V. parahaemolyticus expressing the T3SS2 regulator VtrB or the adhesin Afa-I, infected in the presence of 10mM fucose, or infected with a V. parahaemolyticus strain lacking MAM7, MshA1 and VpadF. (C) Translocation of the T3SS2 effector VopT fused to adenylate cyclase after a 45-minute infection of HT-29 cells +/− 50mM 2-FF, SLC35C1 mutant cells, or CHO cells +/− FUT4. See also Figure S6B. (D) Immunoblot of T3SS2 translocon components VopB2 and VopD2 in host cell membranes after infection with T3SS2+ V. parahaemolyticus. Blots were also probed with antibodies against the host membrane protein calnexin (loading/fractionation control) and bacterial RNAP, demonstrating absence of contaminating intact bacteria. Data are mean with SEM (n=3). P values (** < 0.001, *** < 0.0001) are based on one-way ANOVA with Dunnet post test correction.