The LysR-type regulator QseA regulates both characterized and putative virulence genes in enterohaemorrhagic Escherichia coli O157:H7

Melissa M. Kendall, David A. Rasko, Vanessa Sperandio

Research output: Contribution to journalArticle

28 Scopus citations

Abstract

Enterohaemorrhagic Escherichia coli (EHEC) colonizes the large intestine, causing attaching and effacing (AE) lesions. Most of the genes involved in AE lesion formation are encoded within a chromosomal pathogenicity island termed the locus of enterocyte effacement (LEE). The LysR-type transcriptional factor QseA regulates the LEE by binding to the regulatory region of ler. We performed transcriptome analyses comparing wild-type (WT) EHEC and the qseA mutant to elucidate QseA's role in gene regulation. During both growth phases, several genes carried in O-islands were activated by QseA, whereas genes involved in cell metabolism were repressed. During late-logarithmic growth, QseA activated expression of the LEE genes as well as non-LEE-encoded effector proteins. We also performed electrophoretic mobility shift assays, competition experiments and DNase I footprints. The results demonstrated that QseA directly binds both the ler proximal and distal promoters, its own promoter, as well as promoters of genes encoded in EHEC-specific O-islands. Additionally, we mapped the transcriptional start site of qseA, leading to the identification of two promoter sequences. Taken together, these results indicate that QseA acts as a global regulator in EHEC, co-ordinating expression of virulence genes.

Original languageEnglish (US)
Pages (from-to)1306-1321
Number of pages16
JournalMolecular Microbiology
Volume76
Issue number5
DOIs
StatePublished - Jun 1 2010

ASJC Scopus subject areas

  • Microbiology
  • Molecular Biology

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