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Applied and Environmental Microbiology, November 2004, p. 6435-6443, Vol. 70, No. 11
0099-2240/04/$08.00+0     DOI: 10.1128/AEM.70.11.6435-6443.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Survival of Shewanella oneidensis MR-1 after UV Radiation Exposure

Xiaoyun Qiu,1 George W. Sundin,1,2 Benli Chai,1 and James M. Tiedje1*

Center for Microbial Ecology,1 Department of Plant Pathology, Michigan State University, East Lansing, Michigan2

Received 16 March 2004/ Accepted 7 July 2004

We systematically investigated the physiological response as well as DNA damage repair and damage tolerance in Shewanella oneidensis MR-1 following UVC, UVB, UVA, and solar light exposure. MR-1 showed the highest UVC sensitivity among Shewanella strains examined, with D37 and D10 values of 5.6 and 16.5% of Escherichia coli K-12 values. Stationary cells did not show an increased UVA resistance compared to exponential-phase cells; instead, they were more sensitive at high UVA dose. UVA-irradiated MR-1 survived better on tryptic soy agar than Luria-Bertani plates regardless of the growth stage. A 20% survival rate of MR-1 was observed following doses of 3.3 J of UVC m–2, 568 J of UVB m–2, 25 kJ of UVA m–2, and 558 J of solar UVB m–2, respectively. Photoreactivation conferred an increased survival rate to MR-1 of as much as 177- to 365-fold, 11- to 23-fold, and 3- to 10-fold following UVC, UVB, and solar light irradiation, respectively. A significant UV mutability to rifampin resistance was detected in both UVC- and UVB-treated samples, with the mutation frequency in the range of 10–5 to 10–6. Unlike in E. coli, the expression levels of the nucleotide excision repair (NER) component genes uvrA, uvrB, and uvrD were not damage inducible in MR-1. Complementation of Pseudomonas aeruginosa UA11079 (uvrA deficient) with uvrA of MR-1 increased the UVC survival of this strain by more than 3 orders of magnitude. Loss of damage inducibility of the NER system appears to contribute to the high sensitivity of this bacterium to UVR as well as to other DNA-damaging agents.

* Corresponding author. Mailing address: Center for Microbial Ecology, PSSB 540, Michigan State University, East Lansing, MI 48824. Phone: (517) 353-9021. Fax: (517) 353-2917. E-mail: tiedjej{at}msu.edu.

Applied and Environmental Microbiology, November 2004, p. 6435-6443, Vol. 70, No. 11
0099-2240/04/$08.00+0     DOI: 10.1128/AEM.70.11.6435-6443.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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