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Infect. Immun. doi:10.1128/IAI.02003-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

QseA directly activates transcription of LEE1 in enterohemorrhagic E. coli (EHEC)

Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, 75390-9048, USA

^* To whom correspondence should be addressed. Email: Vanessa.Sperandio{at}UTSouthwestern.edu.

	Abstract

Quorum sensing (QS) in enterohemorrhagic Escherichia coli (EHEC) regulates expression of the locus of enterocyte effacement (LEE). The LEE contains five major operons named LEE1 -5. QseA was previously shown to be activated through QS and to activate the transcription of LEE1. The LEE1 operon encodes Ler, the transcription activator of all other LEE genes and has two promoters: a distal promoter (P1) and a proximal promoter (P2). We have previously reported that QseA acts on P1 and not P2. To identify the minimal region of LEE1 that is necessary for QseA-mediated activation, a series of nested deletion constructs of the LEE1 promoter fused to a lacZ reporter were constructed in both EHEC and E. coli K-12 backgrounds. In an EHEC background, QseA-dependent activation of LEE1 can be observed for the entire regulatory region (beginning on nucleotide -393) until nucleotide -123. In contrast to EHEC, in K-12 there was no QseA-dependent activation of LEE1 transcription between base pairs -393 and -343. These data indicate that a QseA-dependent EHEC-specific regulator is required for the transcription activation of this region. We also observe QseA-dependent LEE1 activation from nucleotides -218 to -123 in K-12, similar to the nested deletion analysis performed in EHEC. Eletrophoretic mobility shift experiments (EMSA) established that QseA directly binds to the -173 to -42 region of LEE1 and not to the -393 to -343 region. These studies suggest that QseA activates transcription of LEE1 by directly binding upstream of its P1 promoter region.

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