Transcriptional Regulation of the
            <i>esp</i>
            Genes of Enterohemorrhagic
            <i>Escherichia coli</i>

Beltrametti, Fabrizio; Kresse, Andreas U.; Guzmán, Carlos A.

doi:10.1128/jb.181.11.3409-3418.1999

Cited by 107 publications

(63 citation statements)

References 47 publications

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“…Similar results were observed in at least four other experiments. tivation in serum-free cell culture medium, instead of LB, has been previously shown to 'pre-induce' the ability of EHEC to signal to host cells (Beltrametti et al, 1999). The abilities of wild type and dam-deficient EHEC to stimulate actin assembly were therefore also compared after growth under these conditions.…”

Section: Resultsmentioning

confidence: 99%

Increased adherence and actin pedestal formation by dam‐deficient enterohaemorrhagic Escherichia coli O157:H7

Campellone

Roe

Løbner‐Olesen

et al. 2007

Molecular Microbiology

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SummaryEnterohaemorrhagic Escherichia coli (EHEC) are highly infectious pathogens capable of causing severe diarrhoeal illnesses. As a critical step during their colonization, EHEC adhere intimately to intestinal epithelial cells and generate F-actin 'pedestal' structures that elevate them above surrounding cell surfaces. Intimate adhesion and pedestal formation result from delivery of the EHEC type III secretion system (TTSS) effector proteins Tir and EspF U into the host cell and expression of the bacterial outer membrane adhesin, intimin. To investigate a role for DNA methylation during the regulation of adhesion and pedestal formation in EHEC, we deleted the dam (DNA adenine methyltransferase) gene from EHEC O157:H7 and demonstrate that this mutation results in increased interactions with cultured host cells. EHECDdam exhibits dramatically elevated levels of adherence and pedestal formation when compared with wild-type EHEC, and expresses significantly higher protein levels of intimin, Tir and EspF U. Analyses of GFP fusions, Northern blotting, reverse transcription polymerase chain reaction, and microarray experiments indicate that the abundance of Tir in the dam mutant is not due to increased transcription levels, raising the possibility that Dam methylation can indirectly control protein expression by a posttranscriptional mechanism. In contrast to other dam-deficient pathogens, EHECDdam is capable of robust intestinal colonization of experimentally infected animals.

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Section: Resultsmentioning

confidence: 99%

Increased adherence and actin pedestal formation by dam‐deficient enterohaemorrhagic Escherichia coli O157:H7

Campellone

Roe

Løbner‐Olesen

et al. 2007

Molecular Microbiology

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“…The environmental cues such as osmolarity, temperature, pH, oxygen, and ions are some of the important signals that bacterial pathogens use to turn-on or turn-off expression of genes critical for colonization and infection in the host. Recent studies have shown that growth of EHEC O157:H7 in media containing high salt concentrations and incubation temperature of 37°C, conditions that closely resemble the intestinal environment, induces the expression of LEE4 operon [37]. It has also been proposed that quorum-sensing signals produced by the normal flora E. coli of the large intestine may represent one of the chemical cues for activating LEE in the early stages of infection [20].…”

Section: Discussionmentioning

confidence: 99%

Hyperadherence of anhhamutant ofEscherichia coliO157:H7 is correlated with enhanced expression of LEE-encoded adherence genes

Sharma

Carlson

Casey

2005

FEMS Microbiology Letters

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Enterohemorrhagic Escherichia coli (EHEC) O157:H7 virulence factors, specifically those conferring intimate adherence to and formation of attaching and effacing lesions (A/E) on host cells, are encoded by a horizontally acquired locus of enterocyte effacement (LEE). Expression of several LEE-encoded genes, which are organized into operons LEE1 through LEE5, is under the positive regulation of ler, the first gene in the LEE1 operon. We have recently demonstrated that EHEC O157:H7 lacking hha exhibited greater than a 10-fold increase in ler expression and that the repression of ler results from the binding of Hha to the ler promoter. In this report, we show that an hha mutant of EHEC O157:H7 exhibited increased adherence to Hep-2 cells, had increased transcriptional activities of LEE1, LEE2, LEE3, and LEE5 as determined by reverse transcriptase-polymerase chain reaction assays, and expressed LEE5::lac transcriptional fusion at levels that were several-fold higher than that expressed by the parental hha+ strain. These results demonstrate that hha is an important regulatory component of the cascade that governs the expression of LEE operons and the resulting ability of EHEC O157:H7 to intimately adhere to host cells.

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“…In enterohaemorrhagic E. coli, espADB transcription is initiated at a promoter located in the distal end of the upstream gene sepL, giving a 2.8 kb transcript (Beltrametti et al, 1999). In EPEC, on the other hand, it has been proposed that espADB transcripts begin at the sepL promoter and include the sepL gene (Elliott et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Role of the nucleoid‐associated protein Fis in the regulation of virulence properties of enteropathogenic Escherichia coli

Goldberg

Johnson

Hinton

et al. 2001

Molecular Microbiology

112

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Virulence gene expression in enteropathogenic Escherichia coli (EPEC) is governed by a combination of environmental factors and virulence regulators. These factors control the expression of the bundle‐forming pili (BFP), intimin, the type III secretion apparatus and the secreted proteins EspA, EspB, EspD and Tir. Expression of the bfp genes occurs for a short period in early exponential phase during growth in tissue culture medium. The nucleoid‐associated regulator protein, Fis, is also expressed transiently during this period. To determine whether Fis was responsible for the growth phase‐dependent expression of bfp, fis was deleted from the EPEC strain E2348/69S. Paradoxically, the Δfis mutant retained the ability to colonize HEp‐2 cells in a characteristic localized adherence pattern, and Fis was found negatively to regulate the expression of BFP. However, the Δfis mutant failed to induce the accretion of filamentous actin, which is associated with attaching and effacing lesions. Using a combination of Western blotting and a novel multiplex primer extension assay (MPEA), we showed that, although the expression of intimin and Tir was not affected, transcription of the LEE4 operon encoding espADB and the virulence activator, Ler, were found to be Fis dependent.

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Transcriptional Regulation of the esp Genes of Enterohemorrhagic Escherichia coli

Cited by 107 publications

References 47 publications

Increased adherence and actin pedestal formation by dam‐deficient enterohaemorrhagic Escherichia coli O157:H7

Increased adherence and actin pedestal formation by dam‐deficient enterohaemorrhagic Escherichia coli O157:H7

Hyperadherence of anhhamutant ofEscherichia coliO157:H7 is correlated with enhanced expression of LEE-encoded adherence genes

Role of the nucleoid‐associated protein Fis in the regulation of virulence properties of enteropathogenic Escherichia coli

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