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. 2017 Jul 21;7:6135. doi: 10.1038/s41598-017-06415-5

Figure 1.

Figure 1

The rpsA∆A438 polymorphism and rpsA over-expression do not confer PZA resistance in M. tuberculosis. (A) Schematic representation of specialized linkage transduction used to introduce the rpsA∆A438 mutation and corresponding nucleotide sequences of the rpsA locus of respective strains. Wild type and rpsA∆A438 mutant strains were tested for the minimum concentration of PZA that was required to inhibit at least 90% of growth relative to the no drug control (MIC90) over 2 weeks of incubation in supplemented 7H9 medium (pH 5.8). (B) Over-expression of rpsA in M. tuberculosis. qRT-PCR was performed on RNA extracted from M. tuberculosis strains H37Ra and H37Ra pMV206::rpsA. Relative mRNA expression was calculated using sigA transcripts for normalization. All MIC90 determinations (A) and qRT-PCR assays (B) were conducted with at least three independent replicates. Three independent isolates bearing the rpsA∆A438 polymorphism, confirmed by full genome sequencing, were assessed. Error bars represent standard deviation from the mean of three independent biological replicates.