Fig. 6: Mutations and amplification of sdrM are pervasive in clinical isolates evolved for DLX resistance.

a DLX MICs of JE2 (WT) and the two clinical isolates CF001 and CF106. Data shown are the mean ± standard deviation of three biological replicates. Significance is shown for comparison to the WT as tested by a one-way ANOVA with the Holm–Sidak’s test for multiple comparisons (**P = 0.0024, ****P < 0.0001). b The presence of mutations in genes encoding DNA gyrase subunits (gyrA, gyrB) and DNA topoisomerase IV subunits (parC, parE), the three mutant alleles sdrM1*, sdrM2*, and sdrM3*, and a genomic amplification containing sdrM, are shown for populations from intermediate passages of three independently evolved populations of the clinical isolates CF001 and CF106. Source Data for a is provided in the Source Data file.