Fig. 6: Partial reversal of TF mediated rifampicin tolerant and hypersusceptible phenotypes through effector gene knockdown. | Nature Communications

Fig. 6: Partial reversal of TF mediated rifampicin tolerant and hypersusceptible phenotypes through effector gene knockdown.

From: Divergent transcriptional regulation of redox-homeostasis and permeability modulate rifampicin tolerance and sensitivity in Mycobacterium tuberculosis

Fig. 6

Change in CFU counts for ATc induced versus uninduced strain constructs in the absence of rifampicin (X-axis) and upon exposure to steady state 10X MIC of rifampicin for 4 days (closed circles) and 12 days (open circles) (Y axis). A Drug tolerant Rv2887 TFI strain (red) compared to icl1 (tolerance effector gene when induced) knockdown (KD) strain (gray) and the double transformant Rv2887 induced plus icl1 KD strain (orange). B Hypersusceptible Rv3736 TFI strain (green) compared to Rv3083 KD strain (gray) and double transformant Rv3736 induced plus Rv3083 KD strain (orange). In both cases, the single KD strains show a phenotype that is opposite to their respective TFI strain (in which the effector gene is positively regulated), while the respective double transformant (TFI induced - effector gene KD) strains show a partial reversal of their respective TFI strain phenotype. Data obtained from three biological replicates. The mean CFU from replicates was used to estimate the fold difference with and without ATc induction.

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