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Gene Review

efpA  -  efflux protein

Mycobacterium tuberculosis CDC1551

 
 
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Disease relevance of efpA

 

High impact information on efpA

  • This gene, lfrA, encodes a putative membrane efflux pump of the major facilitator family, which appears to recognize the hydrophilic FQ, ethidium bromide, acridine, and some quaternary ammonium compounds [4].
  • This review highlights recent advances in our understanding of efflux-mediated drug resistance in mycobacteria, including the distribution of efflux systems in these organisms, their substrate profiles and their contribution to drug resistance [5].
  • Recent reports have suggested that efflux pumps may also be involved in transporting isoniazid, one of the main drugs used to treat tuberculosis [5].
  • Resistance was due to single point mutations in the catalase-peroxidase gene and to reserpine-inhibitable efflux pumps.Conclusions [6].
  • The resistance level decreased in the presence of the efflux pump inhibitors reserpine and CCCP (carbonyl cyanide m-chlorophenylhydrazone) [7].
 

Chemical compound and disease context of efpA

 

Biological context of efpA

 

Anatomical context of efpA

 

Associations of efpA with chemical compounds

  • The deletion of the efpA homologue also produced increased susceptibility to these agents but unexpectedly also resulted in decreased susceptibility to rifamycins, isoniazid, and chloramphenicol (two- to fourfold increase in MICs) [9].
  • In addition, we have identified two groups of genes, possibly forming efflux and detoxification systems, through which M. tuberculosis may limit the effects of triclosan [13].
  • The resistance level decreased in the presence of the efflux pump inhibitors reserpine, carbonyl cyanide m-chlorophenylhydrazone, and verapamil [11].
  • Multidrug-resistant single-step mutants, independent of LfrA and attributed to a yet-unidentified drug efflux pump (here called LfrX), were selected in vitro and showed decreased accumulation of norfloxacin, ethidium bromide, and acriflavine in intact cells [9].
  • The sequences of the putative Tap proteins showed 20 to 30% amino acid identity to membrane efflux pumps of the major facilitator superfamily (MFS), mainly tetracycline and macrolide efflux pumps, and to other proteins of unknown function but with similar antibiotic resistance patterns [14].
 

Analytical, diagnostic and therapeutic context of efpA

References

  1. The Mycobacterium tuberculosis iniA gene is essential for activity of an efflux pump that confers drug tolerance to both isoniazid and ethambutol. Colangeli, R., Helb, D., Sridharan, S., Sun, J., Varma-Basil, M., Hazbón, M.H., Harbacheuski, R., Megjugorac, N.J., Jacobs, W.R., Holzenburg, A., Sacchettini, J.C., Alland, D. Mol. Microbiol. (2005) [Pubmed]
  2. Mechanisms of resistance to fluoroquinolones: state-of-the-art 1992-1994. Piddock, L.J. Drugs (1995) [Pubmed]
  3. Ethambutol, a cell wall inhibitor of Mycobacterium tuberculosis, elicits L-glutamate efflux of Corynebacterium glutamicum. Radmacher, E., Stansen, K.C., Besra, G.S., Alderwick, L.J., Maughan, W.N., Hollweg, G., Sahm, H., Wendisch, V.F., Eggeling, L. Microbiology (Reading, Engl.) (2005) [Pubmed]
  4. Efflux pump of the proton antiporter family confers low-level fluoroquinolone resistance in Mycobacterium smegmatis. Takiff, H.E., Cimino, M., Musso, M.C., Weisbrod, T., Martinez, R., Delgado, M.B., Salazar, L., Bloom, B.R., Jacobs, W.R. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  5. Role of mycobacterial efflux transporters in drug resistance: an unresolved question. De Rossi, E., Aínsa, J.A., Riccardi, G. FEMS Microbiol. Rev. (2006) [Pubmed]
  6. Isoniazid's Bactericidal Activity Ceases because of the Emergence of Resistance, Not Depletion of Mycobacterium tuberculosis in the Log Phase of Growth. Gumbo, T., Louie, A., Liu, W., Ambrose, P.G., Bhavnani, S.M., Brown, D., Drusano, G.L. J. Infect. Dis. (2007) [Pubmed]
  7. mmpL7 gene of Mycobacterium tuberculosis is responsible for isoniazid efflux in Mycobacterium smegmatis. Pasca, M.R., Guglierame, P., De Rossi, E., Zara, F., Riccardi, G. Antimicrob. Agents Chemother. (2005) [Pubmed]
  8. Role of acid pH and deficient efflux of pyrazinoic acid in unique susceptibility of Mycobacterium tuberculosis to pyrazinamide. Zhang, Y., Scorpio, A., Nikaido, H., Sun, Z. J. Bacteriol. (1999) [Pubmed]
  9. Efflux pump-mediated intrinsic drug resistance in Mycobacterium smegmatis. Li, X.Z., Zhang, L., Nikaido, H. Antimicrob. Agents Chemother. (2004) [Pubmed]
  10. Characterization of P55, a multidrug efflux pump in Mycobacterium bovis and Mycobacterium tuberculosis. Silva, P.E., Bigi, F., de la Paz Santangelo, M., Romano, M.I., Martín, C., Cataldi, A., Aínsa, J.A. Antimicrob. Agents Chemother. (2001) [Pubmed]
  11. Rv2686c-Rv2687c-Rv2688c, an ABC fluoroquinolone efflux pump in Mycobacterium tuberculosis. Pasca, M.R., Guglierame, P., Arcesi, F., Bellinzoni, M., De Rossi, E., Riccardi, G. Antimicrob. Agents Chemother. (2004) [Pubmed]
  12. Genomics and the chemotherapy of leprosy. Grosset, J.H., Cole, S.T. Leprosy review. (2001) [Pubmed]
  13. Signature gene expression profiles discriminate between isoniazid-, thiolactomycin-, and triclosan-treated Mycobacterium tuberculosis. Betts, J.C., McLaren, A., Lennon, M.G., Kelly, F.M., Lukey, P.T., Blakemore, S.J., Duncan, K. Antimicrob. Agents Chemother. (2003) [Pubmed]
  14. Molecular cloning and characterization of Tap, a putative multidrug efflux pump present in Mycobacterium fortuitum and Mycobacterium tuberculosis. Aínsa, J.A., Blokpoel, M.C., Otal, I., Young, D.B., De Smet, K.A., Martín, C. J. Bacteriol. (1998) [Pubmed]
 
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