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. 2022 Dec 22;51(1):144–165. doi: 10.1093/nar/gkac1173

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© The Author(s) 2022. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 3. — M. tuberculosis SigH and Mrx2 are involved in the prodrug activation of nNFs. MIC₉₀ values (μg/ml) for the nNF derivatives nNF-C2 and nNF-C4 in the M. tuberculosis H37Rv-wild type strain (wt), M. tuberculosis mrx2 KO mutant (Δmrx2), complemented M. tuberculosis mrx2 KO (Δmrx2::mrx2), M. tuberculosis sigH KO (ΔsigH), and the complemented M. tuberculosis sigH KO (ΔsigH::sigH). mrx2 and sigH KO mutants showed higher resistance to both nNF-C2 and nNF-C4 than the H37Rv_WT, while their complementation with the corresponding wt version of the KO-gene, restored the sensitivity.