Selected Publications
Xu Y, Ehrt S, Schnappinger D, Beites T. Synthetic lethality of Mycobacterium tuberculosis NADH dehydrogenases is due to impaired NADH oxidation. mBio 2023 Dec 19;14(6):e0104523.
Kreutzfeldt KM, Jansen RS, Hartman TE, Gouzy A, Wang R, Krieger IV, Zimmerman MD, Gengenbacher M, Sarathy JP, Xie M, Dartois V, Sacchettini JC, Rhee KY, Schnappinger D, Ehrt S. CinA mediates multidrug tolerance in Mycobacterium tuberculosis. Nat Commun. 2022 Apr 22;13(1):2203.
Beites T, Jansen RS, Wang R, Jinich A, Rhee KY, Schnappinger D, Ehrt S. Multiple acyl-CoA dehydrogenase deficiency kills Mycobacterium tuberculosis in vitro and during infection. Nat Commun. 2021 Nov 15;12(1):6593.
Gouzy, A., Healy, C., Black, K. A., Rhee, K. Y. & Ehrt, S. Growth of Mycobacterium tuberculosis at acidic pH depends on lipid assimilation and is accompanied by reduced GAPDH activity. Proc. Natl. Acad. Sci. USA 118, (2021).
Bosch, B. et al. Genome-wide gene expression tuning reveals diverse vulnerabilities of M. tuberculosis. Cell 184, 4579–4592.e24 (2021).
Su, H. et al. Genetic models of latent tuberculosis in mice reveal differential influence of adaptive immunity. J. Exp. Med. 218, (2021).
Whitaker, M. et al. Two interacting ATPases protect Mycobacterium tuberculosis from glycerol and nitric oxide toxicity. J. Bacteriol. (2020). doi:10.1128/JB.00202-20
Healy, C., Gouzy, A. & Ehrt, S. Peptidoglycan Hydrolases RipA and Ami1 Are Critical for Replication and Persistence of Mycobacterium tuberculosis in the Host. MBio 11, (2020).
Wang, R. et al. Persistent Mycobacterium tuberculosis infection in mice requires PerM for successful cell division. Elife 8, (2019).
Ehrt S, Schnappinger D, Rhee KY. Metabolic principles of persistence and pathogenicity in Mycobacterium tuberculosis. Nat Rev Microbiol. 2018 Aug;16(8):496-507. doi: 10.1038/s41579-018-0013-4. Review. PubMed PMID: 29691481; PubMed Central PMCID: PMC6045436.
Xu W, DeJesus MA, Rücker N, Engelhart CA, Wright MG, Healy C, Lin K, Wang R, Park SW, Ioerger TR, Schnappinger D, Ehrt S. Chemical Genetic Interaction Profiling Reveals Determinants of Intrinsic Antibiotic Resistance in Mycobacterium tuberculosis. Antimicrob Agents Chemother. 2017 Nov 22;61(12). pii:e01334-17. doi: 10.1128/AAC.01334-17. Print 2017 Dec. PubMed PMID: 28893793; PubMed Central PMCID: PMC5700314.
Puckett S, Trujillo C, Wang Z, Eoh H, Ioerger TR, Krieger I, Sacchettini J, Schnappinger D, Rhee KY, Ehrt S. Glyoxylate detoxification is an essential function of malate synthase required for carbon assimilation in Mycobacterium tuberculosis. Proc Natl Acad Sci U S A. 2017 Mar 14;114(11):E2225-E2232. doi:10.1073/pnas.1617655114. Epub 2017 Mar 6. PubMed PMID: 28265055; PubMed Central PMCID: PMC5358392.
Botella H, Vaubourgeix J, Lee MH, Song N, Xu W, Makinoshima H, Glickman MS, Ehrt S. Mycobacterium tuberculosis protease MarP activates a peptidoglycan hydrolase during acid stress. EMBO J. 2017 Feb 15;36(4):536-548. doi:10.15252/embj.201695028. Epub 2017 Jan 5. PubMed PMID: 28057704; PubMed Central PMCID: PMC5437814.
Lin K, O'Brien KM, Trujillo C, Wang R, Wallach JB, Schnappinger D, Ehrt S. Mycobacterium tuberculosis Thioredoxin Reductase Is Essential for Thiol Redox Homeostasis but Plays a Minor Role in Antioxidant Defense. PLoS Pathog. 2016 Jun 1;12(6):e1005675. doi: 10.1371/journal.ppat.1005675. eCollection 2016 Jun. PubMed PMID: 27249779; PubMed Central PMCID: PMC4889078.
Ganapathy U, Marrero J, Calhoun S, Eoh H, de Carvalho LPS, Rhee K, Ehrt S. Two enzymes with redundant fructose bisphosphatase activity sustain gluconeogenesis and virulence in Mycobacterium tuberculosis. Nat Commun. 2015 Aug 10;6:7912. doi: 10.1038/ncomms8912. PubMed PMID: 26258286; PubMed Central PMCID: PMC4535450.
Goodsmith N, Guo XV, Vandal OH, Vaubourgeix J, Wang R, Botella H, Song S, Bhatt K, Liba A, Salgame P, Schnappinger D, Ehrt S. Disruption of an M. tuberculosis membrane protein causes a magnesium-dependent cell division defect and failure to persist in mice. PLoS Pathog. 2015 Feb 6;11(2):e1004645. doi:10.1371/journal.ppat.1004645. eCollection 2015 Feb. PubMed PMID: 25658098; PubMed Central PMCID: PMC4450064.
Puckett S, Trujillo C, Eoh H, Marrero J, Spencer J, Jackson M, Schnappinger D, Rhee K, Ehrt S. Inactivation of fructose-1,6-bisphosphate aldolase prevents optimal co-catabolism of glycolytic and gluconeogenic carbon substrates in Mycobacterium tuberculosis. PLoS Pathog. 2014 May 22;10(5):e1004144. doi:10.1371/journal.ppat.1004144. eCollection 2014 May. PubMed PMID: 24851864; PubMed Central PMCID: PMC4031216.
Marrero J, Rhee KY, Schnappinger D, Pethe K, Ehrt S. Gluconeogenic carbon flow of tricarboxylic acid cycle intermediates is critical for Mycobacterium tuberculosis to establish and maintain infection. Proc Natl Acad Sci U S A. 2010 May 25;107(21):9819-24. doi: 10.1073/pnas.1000715107. Epub 2010 May 3. PubMed PMID: 20439709; PubMed Central PMCID: PMC2906907.
Blumenthal A, Kobayashi T, Pierini LM, Banaei N, Ernst JD, Miyake K, Ehrt S. RP105 facilitates macrophage activation by Mycobacterium tuberculosis lipoproteins. Cell Host Microbe. 2009 Jan 22;5(1):35-46. doi:10.1016/j.chom.2008.12.002. PubMed PMID: 19154986; PubMed Central PMCID:PMC2742161.
Vandal OH, Pierini LM, Schnappinger D, Nathan CF, Ehrt S. A membrane protein preserves intrabacterial pH in intraphagosomal Mycobacterium tuberculosis. Nat Med. 2008 Aug;14(8):849-54. doi: 10.1038/nm.1795. Epub 2008 Jul 20. PubMed PMID: 18641659; PubMed Central PMCID: PMC2538620.