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Journal of Bacteriology, April 2001, p. 2178-2186, Vol. 183, No. 7
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.7.2178-2186.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Global Analysis of Escherichia coli Gene Expression during the Acetate-Induced Acid Tolerance Response

Carrie N. Arnold,dagger Justin McElhanon,Dagger Aaron Lee,§ Ryan Leonhart, and Deborah A. Siegele*

Department of Biology, Texas A&M University, College Station, Texas 77843-3258

Received 22 November 2000/Accepted 17 January 2001

The ability of Escherichia coli to survive at low pH is strongly affected by environmental factors, such as composition of the growth medium and growth phase. Exposure to short-chain fatty acids, such as acetate, proprionate, and butyrate, at neutral or nearly neutral pH has also been shown to increase acid survival of E. coli and Salmonella enterica serovar Typhimurium. To investigate the basis for acetate-induced acid tolerance in E. coli O157:H7, genes whose expression was altered by exposure to acetate were identified using gene arrays. The expression of 60 genes was reduced by at least twofold; of these, 48 encode components of the transcription-translation machinery. Expression of 26 genes increased twofold or greater following treatment with acetate. This included six genes whose products are known to be important for survival at low pH. Five of these genes, as well as six other acetate-induced genes, are members of the E. coli RpoS regulon. RpoS, the stress sigma factor, is known to be required for acid tolerance induced by growth at nonlethal low pH or by entry into stationary phase. Disruption of the rpoS gene by a transposon insertion mutation also prevented acetate-induced acid tolerance. However, induction of RpoS expression did not appear to be sufficient to activate the acid tolerance response. Treatment with either NaCl or sodium acetate (pH 7.0) increased expression of an rpoS::lacZ fusion protein, but only treatment with acetate increased acid survival.

* Corresponding author. Mailing address: Texas A&M University, Biology Department, 3258 TAMU, College Station, TX 77843-3258. Phone: (979) 862-4022. Fax: (979) 845-2891. E-mail: d-siegele{at}tamu.edu.

dagger Present address: Department of Microbiology & Immunology, Stanford University, Stanford, CA 94305.

Dagger Present address: Graduate Division of Biological and Biomedical Sciences, Emory University, Atlanta, GA 30322.

§ Present address: Division of Cell and Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390.

Journal of Bacteriology, April 2001, p. 2178-2186, Vol. 183, No. 7
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.7.2178-2186.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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