An Arm-to-Disarm Strategy to Overcome Phenotypic AMR in .

Most front-line tuberculosis drugs are ineffective against hypoxic non-replicating drug-tolerant () contributing to phenotypic antimicrobial resistance (AMR). This is largely due to the poor permeability in the thick and waxy cell wall of persister cells, leading to diminished drug accumulation and reduced drug-target engagement. Here, using an "arm-to-disarm" prodrug approach, we demonstrate that non-replicating persisters can be sensitized to Moxifloxacin (MXF), a front-line TB drug.

Biosensor-integrated transposon mutagenesis reveals as a coordinator of redox homeostasis in .

() is evolutionarily equipped to resist exogenous reactive oxygen species (ROS) but shows vulnerability to an increase in endogenous ROS (eROS). Since eROS is an unavoidable consequence of aerobic metabolism, understanding how manages eROS levels is essential yet needs to be characterized. By combining the Mrx1-roGFP2 redox biosensor with transposon mutagenesis, we identified 368 genes (redoxosome) responsible for maintaining homeostatic levels of eROS in .