The locus of enterocyte effacement (LEE)-encoded regulator controls expression of both LEE- and non-LEE-encoded virulence factors in enteropathogenic and enterohemorrhagic Escherichia coli

S. J. Elliott, V. Sperandio, J. A. Giron, S. Shin, J. L. Mellies, L. Wainwright, S. W. Hutcheson, T. K. McDaniel, J. B. Kaper

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Abstract

Regulation of virulence gene expression in enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) is incompletely understood. In EPEC, the plasmid-encoded regulator Per is required for maximal expression of proteins encoded on the locus of enterocyte effacement (LEE), and a LEE-encoded regulator (Ler) is part of the Per-mediated regulatory cascade upregulating the LEE2, LEE3, and LEE4 promoters. We now report that Ler is essential for the expression of multiple LEE-located genes in both EPEC and EHEC, including those encoding the type III secretion pathway, the secreted Esp proteins, Tir, and intimin. Ler is therefore central to the process of attaching and effacing (AE) lesion formation. Ler also regulates the expression of LEE-located genes not required for AE-lesion formation, including rorf2, orf10, rorf10, orf19, and espF, indicating that Ler regulates additional virulence properties. In addition, Ler regulates the expression of proteins encoded outside the LEE that are not essential for AE lesion formation, including TagA in EHEC and EspC in EPEC. Δler mutants of both EPEC and EHEC show altered adherence to epithelial cells and express novel fimbriae. Ler is therefore a global regulator of virulence gene expression in EPEC and EHEC.

Original languageEnglish (US)
Pages (from-to)6115-6126
Number of pages12
JournalInfection and Immunity
Volume68
Issue number11
DOIs
StatePublished - 2000

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Enterohemorrhagic Escherichia coli
Enteropathogenic Escherichia coli
Enterocytes
Virulence Factors
Virulence
Proteins
Secretory Pathway
Gene Expression Regulation
Regulator Genes
Genes
Plasmids
Epithelial Cells
Gene Expression

ASJC Scopus subject areas

  • Immunology

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The locus of enterocyte effacement (LEE)-encoded regulator controls expression of both LEE- and non-LEE-encoded virulence factors in enteropathogenic and enterohemorrhagic Escherichia coli. / Elliott, S. J.; Sperandio, V.; Giron, J. A.; Shin, S.; Mellies, J. L.; Wainwright, L.; Hutcheson, S. W.; McDaniel, T. K.; Kaper, J. B.

In: Infection and Immunity, Vol. 68, No. 11, 2000, p. 6115-6126.

Research output: Contribution to journalArticle

Elliott, S. J. ; Sperandio, V. ; Giron, J. A. ; Shin, S. ; Mellies, J. L. ; Wainwright, L. ; Hutcheson, S. W. ; McDaniel, T. K. ; Kaper, J. B. / The locus of enterocyte effacement (LEE)-encoded regulator controls expression of both LEE- and non-LEE-encoded virulence factors in enteropathogenic and enterohemorrhagic Escherichia coli. In: Infection and Immunity. 2000 ; Vol. 68, No. 11. pp. 6115-6126.
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abstract = "Regulation of virulence gene expression in enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) is incompletely understood. In EPEC, the plasmid-encoded regulator Per is required for maximal expression of proteins encoded on the locus of enterocyte effacement (LEE), and a LEE-encoded regulator (Ler) is part of the Per-mediated regulatory cascade upregulating the LEE2, LEE3, and LEE4 promoters. We now report that Ler is essential for the expression of multiple LEE-located genes in both EPEC and EHEC, including those encoding the type III secretion pathway, the secreted Esp proteins, Tir, and intimin. Ler is therefore central to the process of attaching and effacing (AE) lesion formation. Ler also regulates the expression of LEE-located genes not required for AE-lesion formation, including rorf2, orf10, rorf10, orf19, and espF, indicating that Ler regulates additional virulence properties. In addition, Ler regulates the expression of proteins encoded outside the LEE that are not essential for AE lesion formation, including TagA in EHEC and EspC in EPEC. Δler mutants of both EPEC and EHEC show altered adherence to epithelial cells and express novel fimbriae. Ler is therefore a global regulator of virulence gene expression in EPEC and EHEC.",
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AU - Elliott, S. J.

AU - Sperandio, V.

AU - Giron, J. A.

AU - Shin, S.

AU - Mellies, J. L.

AU - Wainwright, L.

AU - Hutcheson, S. W.

AU - McDaniel, T. K.

AU - Kaper, J. B.

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