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Journal of Bacteriology, June 2007, p. 4359-4366, Vol. 189, No. 12
0021-9193/07/$08.00+0 doi:10.1128/JB.00132-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
,
Elke Küster-Schöck,
Thomas A. Auchtung,¶ and
Alan D. Grossman*
Department of Biology, Building 68-530, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139
Received 26 January 2007/ Accepted 2 April 2007
The structural maintenance of chromosome (Smc) protein is highly conserved and involved in chromosome compaction, cohesion, and other DNA-related processes. In Bacillus subtilis, smc null mutations cause defects in DNA supercoiling, chromosome compaction, and chromosome partitioning. We investigated the effects of smc mutations on global gene expression in B. subtilis using DNA microarrays. We found that an smc null mutation caused partial induction of the SOS response, including induction of the defective prophage PBSX. Analysis of SOS and phage gene expression in single cells indicated that approximately 1% of smc mutants have fully induced SOS and PBSX gene expression while the other 99% of cells appear to have little or no expression. We found that induction of PBSX was not responsible for the chromosome partitioning or compaction defects of smc mutants. Similar inductions of the SOS response and PBSX were observed in cells depleted of topoisomerase I, an enzyme that relaxes negatively supercoiled DNA.
Published ahead of print on 6 April 2007.
Supplemental material for this article may be found at http://jb.asm.org/.
Present address: Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824.
Present address: Department of Biology, McGill University, Montreal, QC, Canada.
¶ Present address: Department of Organismal and Evolutionary Biology, Harvard University, Cambridge, MA 02138.
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