JB
Home Help [Feedback] [For Subscribers] [Archive] [Search] --
JB Accepts, published online ahead of print on 6 April 2007
This Article
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
JB.00132-07v1
189/12/4359    most recent
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 Google Scholar
Google Scholar
Right arrow Articles by Britton, R. A.
Right arrow Articles by Grossman, A. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Britton, R. A.
Right arrow Articles by Grossman, A. D.
J. Bacteriol. doi:10.1128/JB.00132-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

SOS Induction in a Subpopulation of Structural Maintenance of Chromosome (Smc) mutant cells in Bacillus subtilis

Robert A. Britton, Elke Kuester-Schoeck, Thomas A. Auchtung, and Alan D. Grossman*

Department of Biology, Building 68-530, Massachusetts Institute of Technology, Cambridge, MA 02139

* To whom correspondence should be addressed. Email: adg{at}mit.edu.


   Abstract

The structural maintenance of chromosomes (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.







Home Help [Feedback] [For Subscribers] [Archive] [Search] --
Appl. Environ. Microbiol. Infect. Immun. Eukaryot. Cell
Mol. Cell. Biol. J. Virol. Microbiol. Mol. Biol. Rev.
ALL ASM JOURNALS

Copyright © 2007 by the American Society for Microbiology. All rights reserved.