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Journal of Bacteriology, December 2009, p. 7279-7287, Vol. 191, No. 23
0021-9193/09/$08.00+0 doi:10.1128/JB.01047-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
Promoter Strength Properties of the Complete Sigma E Regulon of Escherichia coli and Salmonella enterica
,
Vivek K. Mutalik,1,
Gen Nonaka,1,
Sarah E. Ades,3
Virgil A. Rhodius,1* and
Carol A. Gross1,2*
Department of Microbiology and Immunology,1 Department of Cell and Tissue Biology, University of California at San Francisco, San Francisco, California 94158,2 Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, Pennsylvania 168023
Received 7 August 2009/ Accepted 17 September 2009
The 
E-directed envelope stress response maintains outer membrane homeostasis and is an important virulence determinant upon host infection in Escherichia coli and related bacteria. E is activated by at least two distinct mechanisms: accumulation of outer membrane porin precursors and an increase in the alarmone ppGpp upon transition to stationary phase. Expression of the E regulon is driven from a suite of approximately 60 E-dependent promoters. Using green fluorescent protein fusions to each of these promoters, we dissected promoter contributions to the output of the regulon under a variety of in vivo conditions. We found that the E promoters exhibit a large dynamic range, with a few strong and many weak promoters. Interestingly, the strongest promoters control either transcriptional regulators or functions related to porin homeostasis, the very functions conserved among E. coli and its close relatives. We found that (i) the strength of most promoters is significantly affected by the presence of the upstream (–35 to –65) region of the promoter, which encompasses the UP element, a binding site for the C-terminal domain of the 
-subunit of RNA polymerase; (ii) ppGpp generally activates E promoters, and (iii) E promoters are responsive to changing E holoenzyme levels under physiological conditions, reinforcing the idea that the E regulon is extremely dynamic, enabling cellular adaptation to a constantly changing environment.
* Corresponding author. Mailing address: 600 16th Street, Genentech Hall, S372E, University of California at San Francisco, San Francisco, CA 94158-2517. Phone: (415) 476-4161. Fax: (415) 514-4080. E-mail for C. A. Gross: cgross{at}cgl.ucsf.edu. E-mail for V. A. Rhodius: virgil.rhodius{at}ucsf.edu
Published ahead of print on 25 September 2009.
Supplemental material for this article may be found at http://jb.asm.org/.
Present address: Joint Bioenergy Institute, Physical Biosciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720.
Present address: Ajinomoto Co., Inc., 15-1, Kyobashi 1-chome, Chuo-ku, Tokyo 104-8315, Japan.
Journal of Bacteriology, December 2009, p. 7279-7287, Vol. 191, No. 23
0021-9193/09/$08.00+0 doi:10.1128/JB.01047-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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