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Journal of Bacteriology, December 2008, p. 7985-7993, Vol. 190, No. 24
0021-9193/08/$08.00+0     doi:10.1128/JB.00919-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

DNA Repair of 8-Oxo-7,8-Dihydroguanine Lesions in Porphyromonas gingivalis{triangledown} ,{dagger}

Leroy G. Henry,1* Lawrence Sandberg,2 Kangling Zhang,2 and Hansel M. Fletcher1

Division of Microbiology and Molecular Genetics,1 Division of Biochemistry, School of Medicine, Loma Linda University, Loma Linda, California 923502

Received 3 July 2008/ Accepted 1 October 2008

The persistence of Porphyromonas gingivalis in the inflammatory environment of the periodontal pocket requires an ability to overcome oxidative stress. DNA damage is a major consequence of oxidative stress. Unlike the case for other organisms, our previous report suggests a role for a non-base excision repair mechanism for the removal of 8-oxo-7,8-dihydroguanine (8-oxo-G) in P. gingivalis. Because the uvrB gene is known to be important in nucleotide excision repair, the role of this gene in the repair of oxidative stress-induced DNA damage was investigated. A 3.1-kb fragment containing the uvrB gene was PCR amplified from the chromosomal DNA of P. gingivalis W83. This gene was insertionally inactivated using the ermF-ermAM antibiotic cassette and used to create a uvrB-deficient mutant by allelic exchange. When plated on brucella blood agar, the mutant strain, designated P. gingivalis FLL144, was similar in black pigmentation and beta-hemolysis to the parent strain. In addition, P. gingivalis FLL144 demonstrated no significant difference in growth rate, proteolytic activity, or sensitivity to hydrogen peroxide from that of the parent strain. However, in contrast to the wild type, P. gingivalis FLL144 was significantly sensitive to UV irradiation. The enzymatic removal of 8-oxo-G from duplex DNA was unaffected by the inactivation of the uvrB gene. DNA affinity fractionation identified unique proteins that preferentially bound to the oligonucleotide fragment carrying the 8-oxo-G lesion. Collectively, these results suggest that the repair of oxidative stress-induced DNA damage involving 8-oxo-G may occur by a still undescribed mechanism in P. gingivalis.

* Corresponding author. Mailing address: Division of Microbiology and Molecular Genetics, School of Medicine, Loma Linda University, Loma Linda, CA 92350. Phone: (909) 558-4472. Fax: (909) 558-4035. E-mail: lhenry1{at}llu.edu

{triangledown} Published ahead of print on 10 October 2008.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

Journal of Bacteriology, December 2008, p. 7985-7993, Vol. 190, No. 24
0021-9193/08/$08.00+0     doi:10.1128/JB.00919-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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