Fig. 6.

Disruption of the cell envelope reverses propionate and cholesterol catabolism dependent decrease in RIF efficacy. (A) Normalized growth inhibition of ΔphoPR mutant across increasing concentrations of RIF in minimal media compared to WT. Results shown as means from three biological replicates. (B) Relative sulfolipid abundances of WT, aftB mutant, and ΔphoPR mutant grown in minimal media with 1× butyrate and 0.1× propionate (1× BT+0.1× PP), and cholesterol. Relative sulfolipid abundances were determined by the combined normalized mass spectra intensities from m/z 2,000 to 2,800 for each growth condition. MS spectra intensities were normalized using GM2 ganglioside internal standard and cell density. Results shown as means with SDs from two independent experiments. Significance was calculated using unpaired t test, *P < 0.05, **P < 0.01. (C) Normalized growth inhibition of aftB mutant across increasing concentrations of RIF in minimal media compared to WT. Results shown as means from three biological replicates. (D) Calculated fold change in GR₅₀ values of 1× butyrate and 0.1× propionate (1× BT+0.1× PP) and cholesterol conditions against 1× butyrate alone for WT and mutant strains. Significance was calculated using unpaired t test, **P < 0.01, ***P < 0.001, ****P < 0.0001.