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. Author manuscript; available in PMC: 2020 Apr 18.
Published in final edited form as: Cell Chem Biol. 2019 Feb 21;26(4):559–570.e6. doi: 10.1016/j.chembiol.2019.01.007

Figure 4. Chloramphenicol resistance in E. coli expressing H. influenzae nfsB occurs via a drug-modification mechanism.

Figure 4.

Lag-phase assays of E. coli expressing (A) empty vector or (B) H. influenzae nfsB grown in the presence of increasing concentrations of chloramphenicol ranging from 0 μg/ml to 64 μg/ml. (C) Linear regression of incubation time required to reach half-maximal OD600 plotted against chloramphenicol concentration. The slope of the fit line is 3.12±0.11 with an R2 of 0.998. (D) Growth of chloramphenicol-susceptible E. coli in chloramphenicol media pre-conditioned by empty vector or reductase-expressing E. coli strains. All experiments were performed in triplicate with error bars representing standard deviation when present. Significance at p≤0.0001 (****) was calculated based on triplicate experiments using a one-way ANOVA test with Dunnett’s correction for multiple comparisons and reflect a comparison to vector control.