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J. Bacteriol. doi:10.1128/JB.00083-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Growth-Rate Toxicity Phenotypes and Homeostatic Supercoil Control Differentiate E. coli from Salmonella Typhimurium

Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL-35294-0024 USA

^* To whom correspondence should be addressed. Email: nphiggin{at}uab.edu.

	Abstract

Escherichia coli and Salmonella enterica serovar Typhimurium share a high degree of DNA and amino acid identity for 65% of the homologous genes shared by the two genomes. Yet there are different phenotypes for null mutants in several genes that contribute to DNA condensation and nucleoid formation. The mutant R436-S form of the GyrB has a TS phenotype in Salmonella, showing disruption of supercoiling near the terminus and replicon failure at 42°. But this mutation in E. coli is lethal at the permissive temperature. A unifying hypothesis for why the same mutation in highly conserved homologous genes of different species leads to different physiology focuses on homeotic supercoil control. During rapid growth in mid-log phase, E. coli generates 15% more negative supercoils in pBR322 DNA than Salmonella. Differences in compaction and torsional strain on chromosomal DNA explain a complex set of single gene phenotypes, and provide insight into how supercoiling may modulate epigenetic effects on chromosome structure and function and on prophage behavior in vivo.