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Journal of Bacteriology, March 2001, p. 2081-2085, Vol. 183, No. 6
0021-9193/01/$04.00+0 DOI: 10.1128/JB.183.6.2081-2085.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Role for a Phage Promoter in Shiga Toxin 2 Expression from a Pathogenic Escherichia coli
Strain
Patrick L.
Wagner,1
Melody N.
Neely,2,
Xiaoping
Zhang,1
David W. K.
Acheson,1
Matthew K.
Waldor,1,3 and
David I.
Friedman2,*
Howard Hughes Medical
Institute3 and Division of Geographic
Medicine and Infectious Diseases, Tufts University School of
Medicine, Boston, Massachusetts 021111;
Department of Microbiology and Immunology, University of
Michigan, Ann Arbor, Michigan 481092
Received 1 November 2000/Accepted 3 January 2001
Shiga toxins (Stxs), encoded by the stxA and
stxB genes, are important contributors to the virulence of
Escherichia coli O157:H7 and other Stx-producing E. coli (STEC) strains. The stxA and stxB genes in STEC strains are located on the genomes of resident prophages of the
family immediately downstream of the phage late promoters (pR'). The phage-encoded Q proteins modify RNA
polymerase initiating transcription at the cognate
pR' promoter which creates transcription
complexes that transcend a transcription terminator immediately
downstream of pR' as well as terminator kilobases distal to pR'. To test if this
Q-directed processive transcription plays a role in
stx2AB expression, we constructed a
mutant prophage in an O157:H7 clinical isolate from which
pR' and part of Q were deleted but which has an
intact pStx, the previously described
stx2AB-associated promoter. We
report that production of significant levels of Stx2 in this O157:H7
isolate depends on the pR' promoter. Since
transcription initiating at pR' ultimately
requires activation of the phage lytic cascade, expression of
stx2AB in STEC depends primarily on
prophage induction. By showing this central role for the prophage in
stx2AB expression, our findings
contradict the prevailing assumption that phages serve merely as agents
for virulence gene transfer.
*
Corresponding author. Mailing address: Department of
Microbiology and Immunology, Medical School, 5641 Medical Science
Building II, University of Michigan, Ann Arbor, MI 48109-0620. Phone:
(734) 763-3142. Fax: (734) 764-3562. E-mail:
davidfri{at}umich.edu.

Present address: Department of Molecular Microbiology, Washington
University School of Medicine, St. Louis, MO
63110.
Journal of Bacteriology, March 2001, p. 2081-2085, Vol. 183, No. 6
0021-9193/01/$04.00+0 DOI: 10.1128/JB.183.6.2081-2085.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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