This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Moorthy, S. Articles by Mahadevan, S. Search for Related Content PubMed PubMed Citation Articles by Moorthy, S. Articles by Mahadevan, S.

 Previous Article  |  Next Article 

Journal of Bacteriology, July 2002, p. 4033-4038, Vol. 184, No. 14
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.14.4033-4038.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Differential Spectrum of Mutations That Activate the Escherichia coli bgl Operon in an rpoS Genetic Background

Sudha Moorthy^, and S. Mahadevan^*

Department of Molecular Reproduction, Development, and Genetics, Indian Institute of Science, Bangalore 560012, India

Received 22 January 2002/ Accepted 24 April 2002

The bgl promoter is silent in wild-type Escherichia coli under standard laboratory conditions, and as a result, cells exhibit a ß-glucoside-negative (Bgl^-) phenotype. Silencing is brought about by negative elements that flank the promoter and include DNA structural elements and sequences that interact with the nucleoid-associated protein H-NS. Mutations that confer a Bgl⁺ phenotype arise spontaneously at a detectable frequency. Transposition of DNA insertion elements within the regulatory locus, bglR, constitutes the major class of activating mutations identified in laboratory cultures. The rpoS-encoded ^S, the stationary-phase sigma factor, is involved in both physiological as well as genetic changes that occur in the cell under stationary-state conditions. In an attempt to see if the rpoS status of the cell influences the nature of the mutations that activate the bgl promoter, we analyzed spontaneously arising Bgl⁺ mutants in rpoS⁺ and rpoS genetic backgrounds. We show that the spectrum of activating mutations in rpoS cells is different from that in rpoS⁺ cells. Unlike rpoS⁺ cells, where insertions in bglR are the predominant activating mutations, mutations in hns make up the majority in rpoS cells. The physiological significance of these differences is discussed in the context of survival of natural populations of E. coli.

Present address: Department of Geographic Medicine and Infectious Diseases, New England Medical Center, Boston, MA 02111.

This article has been cited by other articles:

• Madhusudan, S., Paukner, A., Klingen, Y., Schnetz, K. (2005). Independent regulation of H-NS-mediated silencing of the bgl operon at two levels: upstream by BglJ and LeuO and downstream by DnaKJ. Microbiology 151: 3349-3359 [Abstract] [Full Text]