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. 2013 Jan 9;110(4):1470–1475. doi: 10.1073/pnas.1215416110

Fig. 1.

Fig. 1.

VisP promotes resistance to stressors, virulence, and cell envelope remodeling in bacteria. (A) S. Typhimurium WT, ΔvisP, and complemented strains survival of CdCl2 (4 mg mL−1). (B) Survival of HCl (pH 5.0) (C) Survival of HCl (pH 2.5). (D) Survival of H2O2 (34 nmol L−1). (E) Bacterial growth under MgCl2 low (20 μM) and high (200 μM) concentrations. (F) Intramacrophage replication of S. Typhimurium WT, ΔvisP, ΔlpxO, ΔlpxO/visP, and complemented strains (+) in J774 macrophage-like cells. (G) LpxO-mediated modifications on the lipid-A chemical structure. (H) TLC of 32P-labeled lipid-A from E. coli K12 W3110 and WD101 (controls), S. Typhimurium WT, ΔvisP, ΔlpxO, ΔlpxO/visP, and complemented strains. Modifications assessed are aminoarabinose (l-Ara4N), 1-diphosphate (1-PP), phosphoethalonamine (pEtn), double lipid-A modifications (double), and LpxO-mediated dioxigenase (OH). W3110 was the E. coli strain used as a control to visualize lipid-A (1,4 bisphosphorylated) and 1-PP species; WD101 was the E. coli strain used as phosphoethalonamine and lipid-A double controls. *P < 0.01, **P < 0.001.