PMID:20444105
| Citation |
Kendall, MM, Rasko, DA and Sperandio, V (2010) The LysR-type regulator QseA regulates both characterized and putative virulence genes in enterohaemorrhagic Escherichia coli O157:H7. Mol. Microbiol. 76:1306-21 |
|---|---|
| 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. |
| Links |
PubMed PMC2936457 Online version:10.1111/j.1365-2958.2010.07174.x |
| Keywords |
Animals; Bacterial Proteins/genetics; Bacterial Proteins/metabolism; Base Sequence; Escherichia coli O157/genetics; Escherichia coli O157/metabolism; Escherichia coli O157/pathogenicity; Escherichia coli Proteins/genetics; Escherichia coli Proteins/metabolism; Gene Expression Profiling; Gene Expression Regulation, Bacterial; Humans; Microarray Analysis; Molecular Sequence Data; Promoter Regions, Genetic; Trans-Activators/genetics; Trans-Activators/metabolism; Transcription Factors/genetics; Transcription Factors/metabolism; Transcription, Genetic |
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