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Journal of Bacteriology, November 2006, p. 7645-7651, Vol. 188, No. 21
0021-9193/06/$08.00+0 doi:10.1128/JB.00801-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Northwestern University, Feinberg School of Medicine, 303 E. Chicago Ave., Chicago, Illinois 60611
Received 5 June 2006/ Accepted 16 August 2006
The strict human pathogen Neisseria gonorrhoeae is exposed to oxidative damage during infection. N. gonorrhoeae has many defenses that have been demonstrated to counteract oxidative damage. However, recN is the only DNA repair and recombination gene upregulated in response to hydrogen peroxide (H2O2) by microarray analysis and subsequently shown to be important for oxidative damage protection. We therefore tested the importance of RecA and DNA recombination and repair enzymes in conferring resistance to H2O2 damage. recA mutants, as well as RecBCD (recB, recC, and recD) and RecF-like pathway mutants (recJ, recO, and recQ), all showed decreased resistance to H2O2. Holliday junction processing mutants (ruvA, ruvC, and recG) showed decreased resistance to H2O2 resistance as well. Finally, we show that RecA protein levels did not increase as a result of H2O2 treatment. We propose that RecA, recombinational DNA repair, and branch migration are all important for H2O2 resistance in N. gonorrhoeae but that constitutive levels of these enzymes are sufficient for providing protection against oxidative damage by H2O2.
Published ahead of print on 25 August 2006.
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