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Journal of Bacteriology, February 2009, p. 1152-1161, Vol. 191, No. 4
0021-9193/09/$08.00+0 doi:10.1128/JB.01292-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139,1 Department of Molecular, Cellular, and Developmental Biology, University of Michigan, Ann Arbor, Michigan 481092
Received 15 September 2008/ Accepted 25 November 2008
DNA double-strand breaks are particularly deleterious lesions that can lead to genomic instability and cell death. We investigated the SOS response to double-strand breaks in both Escherichia coli and Bacillus subtilis. In E. coli, double-strand breaks induced by ionizing radiation resulted in SOS induction in virtually every cell. E. coli strains incapable of SOS induction were sensitive to ionizing radiation. In striking contrast, we found that in B. subtilis both ionizing radiation and a site-specific double-strand break causes induction of prophage PBSX and SOS gene expression in only a small subpopulation of cells. These results show that double-strand breaks provoke global SOS induction in E. coli but not in B. subtilis. Remarkably, RecA-GFP focus formation was nearly identical following ionizing radiation challenge in both E. coli and B. subtilis, demonstrating that formation of RecA-GFP foci occurs in response to double-strand breaks but does not require or result in SOS induction in B. subtilis. Furthermore, we found that B. subtilis cells incapable of inducing SOS had near wild-type levels of survival in response to ionizing radiation. Moreover, B. subtilis RecN contributes to maintaining low levels of SOS induction during double-strand break repair. Thus, we found that the contribution of SOS induction to double-strand break repair differs substantially between E. coli and B. subtilis.
Published ahead of print on 5 December 2008.
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