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Journal of Bacteriology, June 2005, p. 3693-3697, Vol. 187, No. 11
0021-9193/05/$08.00+0     doi:10.1128/JB.187.11.3693-3697.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Characterization of Pathways Dependent on the uvsE, uvrA1, or uvrA2 Gene Product for UV Resistance in Deinococcus radiodurans

Masashi Tanaka,^1,2, Issay Narumi,² Tomoo Funayama,² Masahiro Kikuchi,² Hiroshi Watanabe,² Tsukasa Matsunaga,³ Osamu Nikaido,³ and Kazuo Yamamoto^1,2*

Department of Biomolecular Sciences, Graduate School of Life Sciences, Tohoku University, Sendai 980-8577,¹ Research Group for Biotechnology Development, Takasaki Radiation Chemistry Research Establishment, Japan Atomic Energy Research Institute, Takasaki 370-1292,² Laboratory of Molecular Human Genetics, Faculty of Pharmaceutical Sciences, Kanazawa University, Kanazawa 920-0934, Japan³

Received 4 February 2005/ Accepted 1 March 2005

The genome of a radiation-resistant bacterium, Deinococcus radiodurans, contains one uvsE gene and two uvrA genes, uvrA1 and uvrA2. Using a series of mutants lacking these genes, we determined the biological significance of these components to UV resistance. The UV damage endonuclease (UvsE)-dependent excision repair (UVER) pathway and UvrA1-dependent pathway show some redundancy in their function to counteract the lethal effects of UV. Loss of these pathways does not cause increased sensitivity to UV mutagenesis, suggesting either that these pathways play no function in inducing mutations or that there are mechanisms to prevent mutation other than these excision repair pathways. UVER efficiently removes both cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone photoproducts (6-4PPs) from genomic DNA. In contrast, the UvrA1 pathway does not significantly contribute to the repair of CPDs but eliminates 6-4PPs. Inactivation of uvrA2 does not result in a deleterious effect on survival, mutagenesis, or the repair kinetics of CPDs and 6-4PPs, indicating a minor role in resistance to UV. Loss of uvsE, uvrA1, and uvrA2 reduces but does not completely abolish the ability to eliminate CPDs and 6-4PPs from genomic DNA. The result indicates the existence of a system that removes UV damage yet to be identified.

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* Corresponding author. Mailing address: Department of Biomolecular Sciences, Graduate School of Life Sciences, Tohoku University, Sendai 980-8577, Japan. Phone: (81)-22-217-5054. Fax: (81)-22-217-5053. E-mail: yamamot{at}mail.tains.tohoku.ac.jp.

Present address: Department of Immunology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8544, Japan.

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Journal of Bacteriology, June 2005, p. 3693-3697, Vol. 187, No. 11
0021-9193/05/$08.00+0     doi:10.1128/JB.187.11.3693-3697.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

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