TY - JOUR
T1 - Modulation of Enteropathogenic Escherichia coli Virulence by Quorum Sensing
AU - Sircili, Marcelo P.
AU - Walters, Matthew
AU - Trabulsi, Luis R.
AU - Sperandio, Vanessa
PY - 2004/4
Y1 - 2004/4
N2 - Enteropathogenic Escherichia coli (EPEC) produces a lesion on epithelial cells called the attaching and effacing (AE) lesion. All genes necessary for AE are encoded within the locus of enterocyte effacement (LEE). EPEC also adheres in a characteristic pattern to epithelial cells by forming microcolonies, usually referred to as localized adherence (LA). LA is mediated by the bundle-forming pilus and flagella. The LEE genes are directly activated by the LEE-encoded regulator (Ler). Transcription of Ler is under the control of Per, integration host factor, Fis, BipA, and quorum sensing (QS), specifically through the luxS system. QS activates expression of the LEE genes in EPEC, with QseA activating transcription of ler. Here we report that transcription of the LEE genes and type III secretion are diminished in both luxS and qseA mutants. Transcription of the LEE genes is affected in both mutants mostly during the mid-exponential phase of growth. Transcription of qseA itself is diminished throughout growth in a luxS mutant and is under autorepression. Furthermore, QS activation of type III secretion is independent of per, given that QseA still activates type III secretion in a per mutant strain. Both mutants are deficient in adherence to epithelial cells and form smaller microcolonies. Several factors may contribute to this abnormal behavior: transcription of LEE genes and type III secretion are diminished, and expression of flagella and Per is altered in both mutants. These results suggest that QS is involved in modulating the regulation of the EPEC virulence genes.
AB - Enteropathogenic Escherichia coli (EPEC) produces a lesion on epithelial cells called the attaching and effacing (AE) lesion. All genes necessary for AE are encoded within the locus of enterocyte effacement (LEE). EPEC also adheres in a characteristic pattern to epithelial cells by forming microcolonies, usually referred to as localized adherence (LA). LA is mediated by the bundle-forming pilus and flagella. The LEE genes are directly activated by the LEE-encoded regulator (Ler). Transcription of Ler is under the control of Per, integration host factor, Fis, BipA, and quorum sensing (QS), specifically through the luxS system. QS activates expression of the LEE genes in EPEC, with QseA activating transcription of ler. Here we report that transcription of the LEE genes and type III secretion are diminished in both luxS and qseA mutants. Transcription of the LEE genes is affected in both mutants mostly during the mid-exponential phase of growth. Transcription of qseA itself is diminished throughout growth in a luxS mutant and is under autorepression. Furthermore, QS activation of type III secretion is independent of per, given that QseA still activates type III secretion in a per mutant strain. Both mutants are deficient in adherence to epithelial cells and form smaller microcolonies. Several factors may contribute to this abnormal behavior: transcription of LEE genes and type III secretion are diminished, and expression of flagella and Per is altered in both mutants. These results suggest that QS is involved in modulating the regulation of the EPEC virulence genes.
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U2 - 10.1128/IAI.72.4.2329-2337.2004
DO - 10.1128/IAI.72.4.2329-2337.2004
M3 - Article
C2 - 15039358
AN - SCOPUS:1842535548
SN - 0019-9567
VL - 72
SP - 2329
EP - 2337
JO - Infection and immunity
JF - Infection and immunity
IS - 4
ER -