Title

Recombinational repair is critical for survival of Escherichia coli exposed to nitric oxide

UMMS Affiliation

Department of Biochemistry and Molecular Pharmacology

Publication Date

2000-12-15

Document Type

Article

Subjects

Carbon-Oxygen Lyases; DNA Damage; DNA Glycosylases; DNA Repair; DNA, Bacterial; DNA-(Apurinic or Apyrimidinic Site) Lyase; Deoxyribonuclease IV (Phage T4-Induced); Escherichia coli; *Escherichia coli Proteins; Mutation; N-Glycosyl Hydrolases; Nitric Oxide; *Recombination, Genetic; Ultraviolet Rays

Disciplines

Biochemistry, Biophysics, and Structural Biology | Pharmacology, Toxicology and Environmental Health

Abstract

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.

DOI of Published Version

10.1128/JB.183.1.131-138.2001

Source

J Bacteriol. 2001 Jan;183(1):131-8. Link to article on publisher's site

Journal/Book/Conference Title

Journal of bacteriology

Related Resources

Link to Article in PubMed

PubMed ID

11114909

Link to Full Text

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