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Journal of Bacteriology, January 2001, p. 131-138, Vol. 183, No. 1
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.1.131-138.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Recombinational Repair Is Critical for Survival of Escherichia coli Exposed to Nitric Oxide

Erik J. Spek,1 Teresa L. Wright,1 Molly S. Stitt,1 Nazbeh R. Taghizadeh,1 Steven R. Tannenbaum,1,2 Martin G. Marinus,3 and Bevin P. Engelward1,*

Division of Bioengineering and Environmental Health1 and Department of Chemistry,2 Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, and Department of Pharmacology and Molecular Toxicology, University of Massachusetts Medical School, Worcester, Massachusetts 016053

Received 10 July 2000/Accepted 6 October 2000

Nitric oxide (NO·) is critical to numerous biological processes, including signal transduction and macrophage-mediated immunity. In this study, we have explored the biological effects of NO·-induced DNA damage on Escherichia coli. The relative importance of base excision repair, nucleotide excision repair (NER), and recombinational repair in preventing NO·-induced toxicity was determined. E. coli strains lacking either NER or DNA glycosylases (including those that repair alkylation damage [alkA tag strain], oxidative damage [fpg nei nth strain], and deaminated cytosine [ung strain]) showed essentially wild-type levels of NO· resistance. However, apyrimidinic/apurinic (AP) endonuclease-deficient cells (xth nfo strain) were very sensitive to killing by NO·, which indicates that normal processing of abasic sites is critical for defense against NO·. In addition, recA mutant cells were exquisitely sensitive to NO·-induced killing. Both SOS-deficient (lexA3) and Holliday junction resolvase-deficient (ruvC) cells were very sensitive to NO·, indicating that both SOS and recombinational repair play important roles in defense against NO·. Furthermore, strains specifically lacking double-strand end repair (recBCD strains) were very sensitive to NO·, which suggests that NO· exposure leads to the formation of double-strand ends. One consequence of these double-strand ends is that NO· induces homologous recombination at a genetically engineered substrate. Taken together, it is now clear that, in addition to the known point mutagenic effects of NO·, it is also important to consider recombination events among the spectrum of genetic changes that NO· can induce. Furthermore, the importance of recombinational repair for cellular survival of NO· exposure reveals a potential susceptibility factor for invading microbes.

* Corresponding author. Mailing address: Division of Bioengineering and Environmental Health, Massachusetts Institute of Technology 56-631, 77 Massachusetts Ave., Cambridge, MA 02139. Phone: (617) 258-0260. Fax: (617) 258-0499. E-mail: bevin{at}mit.edu.

Journal of Bacteriology, January 2001, p. 131-138, Vol. 183, No. 1
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.1.131-138.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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