Mycobacterium tuberculosis membrane and energy metabolism

Mycobacterium tuberculosis membrane and energy metabolism encompasses the essential biochemical pathways and structural components required for the bacterium to generate ATP and maintain its electrochemical membrane potential (Cook et al., 2017, Nature Reviews Microbiology). This system is primarily centered on the oxidative phosphorylation machinery, including the electron transport chain (ETC) and the F1F0-ATP synthase complex (Bald et al., 2017, FEMS Microbiology Reviews). Unlike many other bacteria, Mtb is an obligate aerobe that relies heavily on these respiratory processes for survival, even during periods of dormancy or persistence within host granulomas (Gengenbacher & Kaufmann, 2012, FEMS Microbiology Reviews). Therapeutic agents targeting this system, such as bedaquiline, work by inhibiting specific enzymes like ATP synthase or the cytochrome bc1-aa3 complex, thereby depleting the energy reserves of the pathogen (Andries et al., 2005, Science). Because these metabolic processes are distinct from those in human mitochondria, they represent highly selective and potent targets for treating both drug-sensitive and multi-drug-resistant tuberculosis (Koul et al., 2008, Nature). The maintenance of the proton motive force across the membrane is also a critical aspect of this target area, as it drives various secondary active transport processes essential for viability (Rao et al., 2008, Journal of Bacteriology).

Other names

Mtb bioenergeticsMtb oxidative phosphorylationMtb electron transport chainMtb respiratory chain

Inhibition of ATP synthase, inhibition of the cytochrome bc1-aa3 complex (QcrB), and disruption of the electrochemical gradient across the plasma membrane (Andries et al., 2005; Pethe et al., 2013).