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Loss-of-function mutations in ndh do not confer delamanid, ethionamide, isoniazid, or pretomanid resistance in Mycobacterium tuberculosis .

Sushil PandeyCatherine VilchèzeJim WerngrenArnold BainomugisaMikael MansjöRamona GroenheitPaolo MiottoDaniela Maria CirilloChristopher CoulterAlain R BaulardThomas SchönWilliam R JacobsKamel DjaoutClaudio Umberto Köser
Published in: Antimicrobial agents and chemotherapy (2023)
Results from clinical strains and knockouts of the H37Rv and CDC1551 laboratory strains demonstrated that ndh ( Rv1854c ) is not a resistance-conferring gene for isoniazid, ethionamide, delamanid, or pretomanid in Mycobacterium tuberculosis . This difference in the susceptibility to NAD-adduct-forming drugs compared with other mycobacteria may be driven by differences in the absolute intrabacterial NADH concentration.
Keyphrases
  • mycobacterium tuberculosis
  • escherichia coli
  • pulmonary tuberculosis
  • genome wide
  • gene expression
  • dna methylation
  • transcription factor
  • genome wide identification
  • cell proliferation