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Gene Review

katG  -  catalase-peroxidase

Mycobacterium tuberculosis H37Rv

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Disease relevance of katG

  • We assessed the performance of the Genotype MTBDR line probe assay that offers the simultaneous identification of Mycobacterium tuberculosis and its resistance to rifampin (RIF) and isoniazid (INH) by detecting the most commonly found mutations in the rpoB and katG genes [1].
  • Escherichia coli isolates expressing individually five of the eight katG mutations showed loss of catalase and INH oxidation activities, and isolates carrying any of the five pncA mutations showed no pyrazinamidase activity, indicating that these mutations are associated with INH and PZA resistance, respectively [2].
  • The present study analyzed the frequency of the mutations occurring in codons 315 and 463 in katG gene of Mycobacterium tuberculosis strains, isolated from patients with pulmonary tuberculosis from Silesia, Poland [3].

High impact information on katG

  • Of the 36 isoniazid-resistant strains, 23 had mutations in the katG gene, and 5 of these also had mutations in the inhA gene [4].
  • Overexpression of MtAhpC in isoniazid-resistant strains of M. tuberculosis harboring mutations in the catalase/peroxidase katG gene provides antioxidant protection and may substitute for the lost enzyme activities [5].
  • Interestingly, a furA-lacking strain induced the complex at lower concentrations of INH compared with the control strain, whereas higher INH concentrations were necessary to induce the complex in a strain that lacks katG, suggesting that INH needs to be activated by KatG to induce the KasA-containing complex [6].
  • In order to assess the role of ROS detoxification pathways in MTB virulence, we generated a katG null mutant of MTB, deficient in the KatG catalase-peroxidase-peroxynitritase, and evaluated the mutant's ability to replicate and persist in macrophages and mice [7].
  • In the absence of furA, katG was upregulated, cells became hypersensitive to isoniazid, and full virulence was restored, indicating that furA regulates the transcription of both genes [8].

Chemical compound and disease context of katG

  • Lack of clinical significance for the common arginine-to-leucine substitution at codon 463 of the katG gene in isoniazid-resistant Mycobacterium tuberculosis in Singapore [9].
  • A previous limited study demonstrated that Mycobacterium tuberculosis isolates with a mutation at amino-acid position 315 of katG (Delta315) exhibited high-level resistance to isoniazid and were more frequently resistant to streptomycin [10].

Biological context of katG


Anatomical context of katG

  • The system could detect mutations of the rpoB, katG, and embB genes in DNAs extracted from 45 laboratory strains and from sputum samples of 27 patients with pulmonary TB [13].
  • In this study, we describe a multiplex PCR to detect a AGC-->ACC (serine to threonine) mutation in the katG gene and a -15 C-to-T substitution (inhA(C-15T)) at the 5' end of a presumed ribosome binding site in the promoter of the mabA-inhA operon [14].
  • Although the primary targets of activated isoniazid (INH) are proteins involved in the biosynthesis of cell wall mycolic acids, clinical resistance is dominated by specific point mutations in katG [15].

Associations of katG with chemical compounds

  • Mutations in katG, ahpC, and inhA were associated with rifampin resistance, but only katG315 mutations were associated with ethambutol resistance [16].
  • Sequencing of consecutive isolates identified by the National Tuberculosis Program showed 89% of isoniazid-resistant isolates could be detected by targeting just 2 codons, katG 315 and -15C-->T in the inhA promoter, while rifampin resistance will be more complex to detect, with many different mutation and insertion events in rpoB [17].
  • This promoter mutation occurred alone without katG mutations and was associated with a low level of INH and ethionamide resistance [18].
  • DESIGN: Restriction fragment length polymorphisms of repetitive polymerase chain reaction (PCR) amplification and cloning of PCR products were used as nonintegrative methods to describe the composition of katG, rpsL and embB genotypes involved in resistance to isoniazid, streptomycin and ethambutol, respectively, in the original sample [19].
  • A 35 mer oligonucleotide probe specific for the katG gene of M tuberculosis, 3' end-labelled with digoxigenin, was constructed and hybridised with DNA extracted from 26 clinical isolates of M tuberculosis under high stringency conditions [20].

Regulatory relationships of katG

  • This association suggested that furA might regulate katG and other genes involved in pathogenesis [8].

Other interactions of katG

  • Three of 33 strains (9 %) had no mutations in katG, inhA or ndh, indicating that their resistance was due to a new mechanism of resistance [18].
  • Clinical strains of Mycobacterium tuberculosis can be divided into three principal genetic groups based on the single-nucleotide polymorphisms at the katG gene codon 463 and the gyrA gene codon 95 [21].
  • RFLP analysis for katG and direct DNA sequencing of rpoB and rpsL may be practical methods for routine use in clinical microbiology laboratories or molecular pathology laboratories with good molecular capabilities and autosequencers [22].
  • Transcript mapping showed katG to be expressed from a strong promoter, with consensus -10 and -35 elements, preceding furA [8].
  • The katG S315T substitution and fabG1-inhA -15 C-to-T mutation were identified in 34 and 13 of the 52 INH-resistant isolates, respectively, and none of the INH-sensitive isolates [23].

Analytical, diagnostic and therapeutic context of katG


  1. Performance of the Genotype MTBDR Line Probe Assay for Detection of Resistance to Rifampin and Isoniazid in Strains of Mycobacterium tuberculosis with Low- and High-Level Resistance. Brossier, F., Veziris, N., Truffot-Pernot, C., Jarlier, V., Sougakoff, W. J. Clin. Microbiol. (2006) [Pubmed]
  2. Detection of Multidrug Resistance in Mycobacterium tuberculosis. Sekiguchi, J., Miyoshi-Akiyama, T., Augustynowicz-Kopec, E., Zwolska, Z., Kirikae, F., Toyota, E., Kobayashi, I., Morita, K., Kudo, K., Kato, S., Kuratsuji, T., Mori, T., Kirikae, T. J. Clin. Microbiol. (2007) [Pubmed]
  3. PCR-RFLP analysis of a point mutation in codons 315 and 463 of the katG gene of Mycobacterium tuberculosis isolated from patients in Silesia, Poland. Wojtyczka, R.D., Dworniczak, S., Pacha, J., Idzik, D., Kepa, M., Wydmuch, Z., Głab, S., Bajorek, M., Oklek, K., Kozielski, J. Pol. J. Microbiol. (2004) [Pubmed]
  4. Implications of multidrug resistance for the future of short-course chemotherapy of tuberculosis: a molecular study. Heym, B., Honoré, N., Truffot-Pernot, C., Banerjee, A., Schurra, C., Jacobs, W.R., van Embden, J.D., Grosset, J.H., Cole, S.T. Lancet (1994) [Pubmed]
  5. Structure and mechanism of the alkyl hydroperoxidase AhpC, a key element of the Mycobacterium tuberculosis defense system against oxidative stress. Guimarães, B.G., Souchon, H., Honoré, N., Saint-Joanis, B., Brosch, R., Shepard, W., Cole, S.T., Alzari, P.M. J. Biol. Chem. (2005) [Pubmed]
  6. Inhibition of InhA activity, but not KasA activity, induces formation of a KasA-containing complex in mycobacteria. Kremer, L., Dover, L.G., Morbidoni, H.R., Vilchèze, C., Maughan, W.N., Baulard, A., Tu, S.C., Honoré, N., Deretic, V., Sacchettini, J.C., Locht, C., Jacobs, W.R., Besra, G.S. J. Biol. Chem. (2003) [Pubmed]
  7. Role of KatG catalase-peroxidase in mycobacterial pathogenesis: countering the phagocyte oxidative burst. Ng, V.H., Cox, J.S., Sousa, A.O., MacMicking, J.D., McKinney, J.D. Mol. Microbiol. (2004) [Pubmed]
  8. Regulation of catalase-peroxidase (KatG) expression, isoniazid sensitivity and virulence by furA of Mycobacterium tuberculosis. Pym, A.S., Domenech, P., Honoré, N., Song, J., Deretic, V., Cole, S.T. Mol. Microbiol. (2001) [Pubmed]
  9. Lack of clinical significance for the common arginine-to-leucine substitution at codon 463 of the katG gene in isoniazid-resistant Mycobacterium tuberculosis in Singapore. Lee, A.S., Tang, L.L., Lim, I.H., Ling, M.L., Tay, L., Wong, S.Y. J. Infect. Dis. (1997) [Pubmed]
  10. Public health impact of isoniazid-resistant Mycobacterium tuberculosis strains with a mutation at amino-acid position 315 of katG: a decade of experience in The Netherlands. van Doorn, H.R., de Haas, P.E., Kremer, K., Vandenbroucke-Grauls, C.M., Borgdorff, M.W., van Soolingen, D. Clin. Microbiol. Infect. (2006) [Pubmed]
  11. Genotypic Analysis of Multidrug-Resistant Mycobacterium tuberculosis Isolates Recovered From Central China. Zhang, S.L., Qi, H., Qiu, D.L., Li, D.X., Zhang, J., Du, C.M., Wang, G.B., Yang, Z.R., Sun, Q. Biochem. Genet. (2007) [Pubmed]
  12. Mutations in the rpoB and katG genes leading to drug resistance in Mycobacterium tuberculosis in Latvia. Tracevska, T., Jansone, I., Broka, L., Marga, O., Baumanis, V. J. Clin. Microbiol. (2002) [Pubmed]
  13. Dual-probe assay for rapid detection of drug-resistant Mycobacterium tuberculosis by real-time PCR. Wada, T., Maeda, S., Tamaru, A., Imai, S., Hase, A., Kobayashi, K. J. Clin. Microbiol. (2004) [Pubmed]
  14. New multiplex PCR for rapid detection of isoniazid-resistant Mycobacterium tuberculosis clinical isolates. Herrera-León, L., Molina, T., Saíz, P., Sáez-Nieto, J.A., Jiménez, M.S. Antimicrob. Agents Chemother. (2005) [Pubmed]
  15. The genetics and biochemistry of isoniazid resistance in mycobacterium tuberculosis. Slayden, R.A., Barry, C.E. Microbes Infect. (2000) [Pubmed]
  16. Population genetics study of isoniazid resistance mutations and evolution of multidrug-resistant Mycobacterium tuberculosis. Hazbón, M.H., Brimacombe, M., Bobadilla del Valle, M., Cavatore, M., Guerrero, M.I., Varma-Basil, M., Billman-Jacobe, H., Lavender, C., Fyfe, J., García-García, L., León, C.I., Bose, M., Chaves, F., Murray, M., Eisenach, K.D., Sifuentes-Osornio, J., Cave, M.D., Ponce de León, A., Alland, D. Antimicrob. Agents Chemother. (2006) [Pubmed]
  17. Mutations prevalent among rifampin- and isoniazid-resistant Mycobacterium tuberculosis isolates from a hospital in Vietnam. Caws, M., Duy, P.M., Tho, D.Q., Lan, N.T., Hoa, D.V., Farrar, J. J. Clin. Microbiol. (2006) [Pubmed]
  18. Molecular characterization of isoniazid-resistant clinical isolates of Mycobacterium tuberculosis from the USA. Guo, H., Seet, Q., Denkin, S., Parsons, L., Zhang, Y. J. Med. Microbiol. (2006) [Pubmed]
  19. Heteroresistance in Mycobacterium tuberculosis. Rinder, H., Mieskes, K.T., Löscher, T. The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease. (2001) [Pubmed]
  20. Presence of katG gene in resistant Mycobacterium tuberculosis. Jaber, M., Rattan, A., Kumar, R. J. Clin. Pathol. (1996) [Pubmed]
  21. Association between Mycobacterium tuberculosis Beijing/W Lineage Strain Infection and Extrathoracic Tuberculosis: Insights from Epidemiologic and Clinical Characterization of the Three Principal Genetic Groups of M. tuberculosis Clinical Isolates. Kong, Y., Cave, M.D., Zhang, L., Foxman, B., Marrs, C.F., Bates, J.H., Yang, Z.H. J. Clin. Microbiol. (2007) [Pubmed]
  22. Detection of resistance to isoniazid, rifampin, and streptomycin in clinical isolates of Mycobacterium tuberculosis by molecular methods. Nachamkin, I., Kang, C., Weinstein, M.P. Clin. Infect. Dis. (1997) [Pubmed]
  23. Molecular characterization of isoniazid-resistant Mycobacterium tuberculosis isolates collected in Australia. Lavender, C., Globan, M., Sievers, A., Billman-Jacobe, H., Fyfe, J. Antimicrob. Agents Chemother. (2005) [Pubmed]
  24. Rapid genotypic detection of rifampin- and isoniazid-resistant Mycobacterium tuberculosis directly in clinical specimens. Bang, D., Bengård Andersen, A., Thomsen, V.Ø. J. Clin. Microbiol. (2006) [Pubmed]
  25. Molecular analysis of isoniazid resistance in Mycobacterium tuberculosis isolates recovered from South Korea. Kim, S.Y., Park, Y.J., Kim, W.I., Lee, S.H., Ludgerus Chang, C., Kang, S.J., Kang, C.S. Diagn. Microbiol. Infect. Dis. (2003) [Pubmed]
  26. Prevalence of katG Ser315 substitution and rpoB mutations in isoniazid-resistant Mycobacterium tuberculosis isolates from Brazil. Höfling, C.C., Pavan, E.M., Giampaglia, C.M., Ferrazoli, L., Aily, D.C., de Albuquerque, D.M., Ramos, M.C. The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease. (2005) [Pubmed]
  27. Strain variation in the katG region of Mycobacterium tuberculosis. Zhang, Y., Young, D. Mol. Microbiol. (1994) [Pubmed]
  28. Effect of katG mutations on the virulence of Mycobacterium tuberculosis and the implication for transmission in humans. Pym, A.S., Saint-Joanis, B., Cole, S.T. Infect. Immun. (2002) [Pubmed]
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