title: Elevation of Fumarate Levels Compromise Redox Control and Viability in Mycobacterium tuberculosis.
abstract: In this issue of Cell Chemical Biology, Ruecker et al. (2017) show that fumarase depletion in Mycobacterium tuberculosis leads to fumarate, a TCA cycle intermediate, accumulation, causing succination of a range of thiol-containing metabolites and proteins. Fumarate is bactericidal to the pathogen, and its accumulation may enhance the bactericidal effector mechanisms of other TCA cycle intermediates that accumulate due to activation of infected macrophages.
authors.affiliation: Tuberculosis Research Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
authors.forename: Yong-Mo
authors.initials: YM
authors.lastname: Ahn
authors.affiliation: Tuberculosis Research Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: hboshoff@niaid.nih.gov.
authors.forename: Helena I
authors.initials: HI
authors.lastname: Boshoff
mesh_terms: D005649:Fumarate Hydratase / Q000172:deficiency; D005650:Fumarates; D008661:Metabolism, Inborn Errors; D009123:Muscle Hypotonia; D009169:Mycobacterium tuberculosis; D010084:Oxidation-Reduction; D011596:Psychomotor Disorders
chemical_list: D005650:Fumarates; D005649:Fumarate Hydratase