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Journal of Bacteriology, August 2001, p. 4562-4570, Vol. 183, No. 15
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.15.4562-4570.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

DNA Microarray-Mediated Transcriptional Profiling of the Escherichia coli Response to Hydrogen Peroxide

Ming Zheng,1,2 Xunde Wang,1 Lori J. Templeton,2 Dana R. Smulski,2 Robert A. LaRossa,2 and Gisela Storz1,*

Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892,1 and Biochemical Science and Engineering, Central Research and Development, E. I. DuPont de Nemours and Company, Wilmington, Delaware 19880-03282

Received 15 March 2001/Accepted 15 May 2001

The genome-wide transcription profile of Escherichia coli cells treated with hydrogen peroxide was examined with a DNA microarray composed of 4,169 E. coli open reading frames. By measuring gene expression in isogenic wild-type and oxyR deletion strains, we confirmed that the peroxide response regulator OxyR activates most of the highly hydrogen peroxide-inducible genes. The DNA microarray measurements allowed the identification of several new OxyR-activated genes, including the hemH heme biosynthetic gene; the six-gene suf operon, which may participate in Fe-S cluster assembly or repair; and four genes of unknown function. We also identified several genes, including uxuA, encoding mannonate hydrolase, whose expression might be repressed by OxyR, since their expression was elevated in the Delta oxyR mutant strain. In addition, the induction of some genes was found to be OxyR independent, indicating the existence of other peroxide sensors and regulators in E. coli. For example, the isc operon, which specifies Fe-S cluster formation and repair activities, was induced by hydrogen peroxide in strains lacking either OxyR or the superoxide response regulators SoxRS. These results expand our understanding of the oxidative stress response and raise interesting questions regarding the nature of other regulators that modulate gene expression in response to hydrogen peroxide.

* Corresponding author. Mailing address: NIH, Building 18T, Room 101, 18 Library Dr., MSC 5430, Bethesda, MD 20892-5430. Phone: (301) 402-0968. Fax: (301) 402-0078. E-mail: storz{at}helix.nih.gov.

Journal of Bacteriology, August 2001, p. 4562-4570, Vol. 183, No. 15
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.15.4562-4570.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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