This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow An erratum has been published
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zeibell, K.
Right arrow Articles by Miller, J. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zeibell, K.
Right arrow Articles by Miller, J. H.

 Previous Article  |  Next Article 

Journal of Bacteriology, March 2007, p. 2331-2338, Vol. 189, No. 6
0021-9193/07/$08.00+0     doi:10.1128/JB.01656-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Mutagenesis and Repair in Bacillus anthracis: the Effect of Mutators{triangledown}

Krystle Zeibell, Sharon Aguila, Vivian Yan Shi, Andrea Chan, Hanjing Yang, and Jeffrey H. Miller*

Department of Microbiology, Immunology, and Molecular Genetics, and The Molecular Biology Institute, University of California, Los Angeles, California 90095

Received 25 October 2006/ Accepted 21 December 2006

We have generated mutator strains of Bacillus anthracis Sterne by using directed gene knockouts to investigate the effect of deleting genes involved in mismatch repair, oxidative repair, and maintaining triphosphate pools. The single-knockout strains are deleted for mutS, mutY, mutM, or ndk. We also made double-knockout strains that are mutS ndk or mutY mutM. We have measured the levels of mutations in the rpoB gene that lead to the Rifr phenotype and have examined the mutational specificity. In addition, we examined the mutational specificity of two mutagens, 5-azacytidine and N-methyl-N'-nitro-N-nitroso-guanidine. The mutY and mutM single knockouts are weak mutators by themselves, but the combination of mutY mutM results in very high mutation rates, all due to G:C -> T:A transversions. The situation parallels that seen in Escherichia coli. Also, mutS knockouts are strong mutators and even stronger in the presence of a deletion of ndk. The number of sites in rpoB that can result in the Rifr phenotype by single-base substitution is more limited than in certain other bacteria, such as E. coli and Deinococcus radiodurans, although the average mutation rate per mutational site is roughly comparable. Hotspots at sites with virtually identical surrounding sequences are organism specific.


* Corresponding author. Mailing address: Department of MIMG/UCLA, 1602 Molecular Sciences Bldg., 405 Hilgard Ave., Los Angeles, CA 90095. Phone: (310) 825-8460. Fax: (310) 206-3088. E-mail: jhmiller{at}microbio.ucla.edu.

{triangledown} Published ahead of print on 12 January 2007.


Journal of Bacteriology, March 2007, p. 2331-2338, Vol. 189, No. 6
0021-9193/07/$08.00+0     doi:10.1128/JB.01656-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Nordman, J., Wright, A. (2008). The relationship between dNTP pool levels and mutagenesis in an Escherichia coli NDP kinase mutant. Proc. Natl. Acad. Sci. USA 105: 10197-10202 [Abstract] [Full Text]  
  • Marcobal, A. M., Sela, D. A., Wolf, Y. I., Makarova, K. S., Mills, D. A. (2008). Role of Hypermutability in the Evolution of the Genus Oenococcus. J. Bacteriol. 190: 564-570 [Abstract] [Full Text]