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Journal of Bacteriology, June 2006, p. 3837-3848, Vol. 188, No. 11
0021-9193/06/$08.00+0     doi:10.1128/JB.00239-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

The Superoxide Dismutases of Bacillus anthracis Do Not Cooperatively Protect against Endogenous Superoxide Stress

Karla D. Passalacqua,1 Nicholas H. Bergman,1,2 Amy Herring-Palmer,1 and Philip Hanna1*

Department of Microbiology and Immunology,1 Bioinformatics Program, University of Michigan Medical School, Ann Arbor, Michigan 481092

Received 15 February 2006/ Accepted 13 March 2006

The Bacillus anthracis chromosome encodes four unique, putative superoxide dismutase (sod) genes. During exponential growth and sporulation, sodA1, sodA2, and sodC are transcribed constitutively throughout the growth cycle as individual genes. In contrast, the transcription of sod15 occurs mainly during late exponential and sporulation phases as part of a four-gene operon that may be involved in spore formation. Vegetative cell and spore lysates of wild-type Sterne and superoxide dismutase deletion ({Delta}sod) mutants show detectable SOD activity for SODA1 and SODA2, and protein analysis suggests that these two proteins form active homodimers and heterodimers. A comparison of the growth of parental versus {Delta}sod mutants under various chemical oxidative stresses indicates that {Delta}sodA1 mutants are particularly sensitive to endogenously produced superoxide, whereas {Delta}sodA2, {Delta}sod15, and {Delta}sodC mutants remain as resistant to this stress as the parental strain. In addition, in mouse survival assays, {Delta}sod15 and {Delta}sodA1 were responsible for less end-point death, but the level of decreased virulence does not fall within a statistically significant range. Collectively, these data show that sodA1 acts as a major protectant from intracellular superoxide stress, that sod15 is transcribed as part of an operon that may play a role in cell morphology, and that sodA2 and sodC may have minor roles that are not apparent in the conditions tested here.


* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Michigan Medical School, 1150 West Medical Center Dr., 6703 Medical Science Building II, Ann Arbor, MI 48109. Phone: (734) 615-3706. Fax: (734) 764-3562. E-mail: pchanna{at}umich.edu.


Journal of Bacteriology, June 2006, p. 3837-3848, Vol. 188, No. 11
0021-9193/06/$08.00+0     doi:10.1128/JB.00239-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




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