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Title: A role for 16S rRNA dimethyltransferase (ksgA) in intrinsic clarithromycin resistance in Mycobacterium tuberculosis
Authors: Saranya Phunpruch
Saradee Warit
Rungaroon Suksamran
Pamaree Billamas
Sarinya Jaitrong
Prasit Palittapongarnpim
Therdsak Prammananan
King Mongkut's Institute of Technology Ladkrabang
Thailand National Center for Genetic Engineering and Biotechnology
Mahidol University
Keywords: Medicine
Issue Date: 1-Jun-2013
Citation: International Journal of Antimicrobial Agents. Vol.41, No.6 (2013), 548-551
Abstract: The emergence of extensively drug-resistant tuberculosis (XDR-TB) makes the control of tuberculosis (TB) difficult. As a result, there is an urgent need to develop new anti-TB drugs. Alternatively, drugs that have already been used in humans as anti-infectives and later found to have antitubercular activity might be useful as anti-TB drugs, particularly against drug-resistant TB. Clarithromycin (CLR), a 14-membered macrolide and protein synthesis inhibitor, has potent activity against most mycobacterial infections, except Mycobacterium tuberculosis. Mycobacterium tuberculosis is naturally resistant to CLR [minimum inhibitory concentration (MIC) of 8-16 μg/mL] owing to the presence of inducible erm methylase (ErmMT). With a view to gaining further insight into the mechanisms of innate CLR resistance in M. tuberculosis, CLR-susceptible M. tuberculosis H37Rv mutants were generated by transposon mutagenesis. One mutant, designated as Tn-196, was further investigated and it was found that ksgA (Rv1010) was inactivated by the transposon. The ksgA gene encodes a 16S rRNA adenine dimethyltransferase that methylates A1518 and A1519 (Escherichia coli numbering) of 16S rRNA and plays an important role in ribosome biogenesis. Complementation of the Tn-196 mutant with a wild-type ksgA gene restored the resistant phenotype (MIC of 8-16 μg/mL), corroborating the association of ksgA with intrinsic CLR resistance in M. tuberculosis. © 2013 Elsevier B.V. and the International Society of Chemotherapy.
ISSN: 18727913
Appears in Collections:Scopus 2011-2015

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