Editor: Rustam Aminov
The role of Bacteroides fragilis RecQ DNA helicases in cell survival after metronidazole exposure
Article first published online: 18 APR 2011
© 2011 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved
FEMS Microbiology Letters
Volume 319, Issue 2, pages 125–132, June 2011
How to Cite
Paul, L., Patrick, S., Nord, C. E. and Abratt, V. (2011), The role of Bacteroides fragilis RecQ DNA helicases in cell survival after metronidazole exposure. FEMS Microbiology Letters, 319: 125–132. doi: 10.1111/j.1574-6968.2011.02271.x
- Issue published online: 17 MAY 2011
- Article first published online: 18 APR 2011
- Accepted manuscript online: 22 MAR 2011 08:42AM EST
- Received 17 February 2011; revised 14 March 2011; accepted 14 March 2011., Final version published online 18 April 2011.
- Bacteroides fragilis;
The inactivation of Bacteroides fragilis genes encoding putative RecQ helicases recQ1, recQ2 and recQ3 (ORFs BF638R_3282, BF638R_3781, BF638R_3932) was used to determine whether these proteins are involved in cell survival following metronidazole exposure. The effects of the mutations on growth, cellular morphology and DNA integrity were also evaluated. Mutations in the RecQ DNA helicases caused increased sensitivity to metronidazole, with recQ1, recQ2 and recQ3 mutants being 1.32-fold, 41.88-fold and 23.18-fold more sensitive than the wild type, respectively. There was no difference in cell growth between the recQ1 and recQ3 mutants and the wild type. However, the recQ2 mutant exhibited reduced cell growth, aberrant cell division and increased pleiomorphism, with an increase in filamentous forms and chains of cells being observed using light, fluorescence and electron microscopy. There was no spontaneous accumulation of DNA single- or double-strand breaks in the recQ mutants, as compared with the wild type, during normal cell growth in the absence of metronidazole. Bacteroides fragilis RecQ DNA helicases, therefore, enhance cell survival following metronidazole damage. The abnormal cellular phenotype and growth characteristics of recQ2 mutant cells suggest that this gene, or the downstream gene of the operon in which it occurs, may be involved in cell division.