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Journal of Bacteriology, September 2004, p. 6179-6185, Vol. 186, No. 18
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.18.6179-6185.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

The Small Noncoding DsrA RNA Is an Acid Resistance Regulator in Escherichia coli{dagger}

Richard A. Lease,1,2* Dorie Smith,1 Kathleen McDonough,1 and Marlene Belfort1

Wadsworth Center, New York State Department of Health, Center for Medical Sciences, Albany, New York,1 Department of Biophysics, The Johns Hopkins University, Baltimore, Maryland2

Received 21 April 2004/ Accepted 18 June 2004

DsrA RNA is a small (87-nucleotide) regulatory RNA of Escherichia coli that acts by RNA-RNA interactions to control translation and turnover of specific mRNAs. Two targets of DsrA regulation are RpoS, the stationary-phase and stress response sigma factor ({sigma}s), and H-NS, a histone-like nucleoid protein and global transcription repressor. Genes regulated globally by RpoS and H-NS include stress response proteins and virulence factors for pathogenic E. coli. Here, by using transcription profiling via DNA arrays, we have identified genes induced by DsrA. Steady-state levels of mRNAs from many genes increased with DsrA overproduction, including multiple acid resistance genes of E. coli. Quantitative primer extension analysis verified the induction of individual acid resistance genes in the hdeAB, gadAX, and gadBC operons. E. coli K-12 strains, as well as pathogenic E. coli O157:H7, exhibited compromised acid resistance in dsrA mutants. Conversely, overproduction of DsrA from a plasmid rendered the acid-sensitive dsrA mutant extremely acid resistant. Thus, DsrA RNA plays a regulatory role in acid resistance. Whether DsrA targets acid resistance genes directly by base pairing or indirectly via perturbation of RpoS and/or H-NS is not known, but in either event, our results suggest that DsrA RNA may enhance the virulence of pathogenic E. coli.

* Corresponding author. Mailing address: Department of Biophysics, Jenkins Hall, Homewood Campus, The Johns Hopkins University, 3400 N. Charles St., Baltimore, MD 21218. Phone: (410) 516-6536. Fax: (410) 516-4118. E-mail: ral{at}jhu.edu.

{dagger} Supplemental material for this article may be found at http://jb.asm.org.

Journal of Bacteriology, September 2004, p. 6179-6185, Vol. 186, No. 18
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.18.6179-6185.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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