Tejan Lodhiya

eLife Assessment In this important work, Lodhiya et al. provide evidence that excessive ATP underlies the killing of the model organism Mycobacterium smegmatis by two mechanistically-distinct antibiotics. The data are generally solid as the authors deploy multiple, orthogonal readouts and methods for manipulating reactive oxygen species and ATP. The work will be of interest to those studying antibiotic mechanisms of action.

Abstract Antibiotic-tolerant bacteria, due to their unique physiology, are refractory to antimicrobial killing and pose challenges for infection control. Incomplete knowledge of how bactericidal antibiotics work limits our understanding of partial resistance from phenotypic tolerance in mycobacteria, a driver for developing genetic resistance.

Abstract Antibiotic-tolerant bacteria, due to their unique physiology, are refractory to antimicrobial killing and pose challenges for successful therapy. M. tuberculosis, the causative agent of tuberculosis (TB), is exceptionally difficult to control due to antibiotic tolerance. Incomplete knowledge of how bactericidal antibiotics work has impeded our understanding of the development of antibiotic tolerance in mycobacteria.