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JAC Advance Access originally published online on September 16, 2008
Journal of Antimicrobial Chemotherapy 2008 62(6):1199-1202; doi:10.1093/jac/dkn387
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Original research

Mycobacterium tuberculosis DNA repair in response to subinhibitory concentrations of ciprofloxacin

D. M. O'Sullivan1,*, J. Hinds2, P. D. Butcher2, S. H. Gillespie1,3 and T. D. McHugh1

1 Centre for Medical Microbiology, Department of Infection, Royal Free Campus, University College London, Rowland Hill Street, Hampstead, London NW3 2PF, UK 2 Bacterial Microarray Group, Division of Cellular and Molecular Medicine, St George's, University of London, Cranmer Terrace, London SW17 0RE, UK 3 Health Protection Agency, Regional Microbiology Network, Holborn Gate, London WC1V 7PP, UK

Received 22 May 2008; returned 7 July 2008; revised 8 August 2008; accepted 18 August 2008

* Corresponding author. Present address. Department of Infectious and Tropical Disease, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK. Tel: +44-20-7927-2468; Fax: +44-20-7637-4314; E-mail: denise.o'sullivan{at}lshtm.ac.uk

Objectives: To investigate how the SOS response, an error-prone DNA repair pathway, is expressed following subinhibitory quinolone treatment of Mycobacterium tuberculosis.

Methods: Genome-wide expression profiling followed by quantitative RT (qRT)–PCR was used to study the effect of ciprofloxacin on M. tuberculosis gene expression.

Results: Microarray analysis showed that 16/110 genes involved in DNA protection, repair and recombination were up-regulated. There appeared to be a lack of downstream genes involved in the SOS response. qRT–PCR detected an induction of lexA and recA after 4 h and of dnaE2 after 24 h of subinhibitory treatment.

Conclusions: The pattern of gene expression observed following subinhibitory quinolone treatment differed from that induced after other DNA-damaging agents (e.g. mitomycin C). The expression of the DnaE2 polymerase response was significantly delayed following subinhibitory quinolone exposure.

Keywords: SOS repair , mutation , gene expression


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