Transcriptional regulation of flhDC by QseBC and σ28 (FliA) in enterohaemorrhagic Escherichia coli

Clarke, Marcie B.; Sperandio, Vanessa

doi:10.1111/j.1365-2958.2005.04849.x

Cited by 47 publications

(76 citation statements)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Due to the key role of flhDC in flagella synthesis, the regulation of its expression has been studied at both the transcriptional and post-transcriptional levels (Soutourina & Bertin, 2003). Many regulatory proteins, such as H-NS (Bertin et al, 1994;Soutourina et al, 1999), cAMP-CAP complex (catabolite gene activator protein) (Soutourina et al, 1999), IHF (Yona-Nadler et al, 2003), OmpR (Kim et al, 2003;Shin & Park, 1995) and QseBC (Clarke & Sperandio, 2005), have been demonstrated to participate in this regulation process. Most of these regulators bind to the regulatory region of flhDC; this region is not well conserved across different bacterial species, suggesting that the regulatory mechanisms may also be different.…”

Section: Introductionmentioning

confidence: 99%

Positive regulation of flhDC expression by OmpR in Yersinia pseudotuberculosis

Wang

Ding

et al. 2009

Microbiology

View full text Add to dashboard Cite

OmpR has been demonstrated to negatively regulate the expression of the flagellar master operon flhDC in a wide variety of bacterial species. Here we report the positive regulation of flhDC expression by OmpR in Yersinia pseudotuberculosis. A s 70 -dependent promoter was identified by primer extension analysis and an active region with two conserved OmpR-binding sites around the flhDC promoter was confirmed. To confirm the regulation of flhDC expression by OmpR, flhDC as well as the downstream flagellar genes fliA, flgD, flgA, flgM, fliC and flaA were fused to lacZ, and decreased expression of all these genes in an ompR mutant (DompR) was detected. Furthermore, DompR was defective in bacterial motility and flagella synthesis. This defect was due to the low level of expression of flhDC in DompR since overproduction of FlhDC in DompR restored bacterial motility. The importance of two conserved OmpR-binding sites around the flhDC promoter region in the regulation of flhDC expression by OmpR was demonstrated by the fact that mutation of either one or both sites significantly decreased the promoter activity in the wild-type but not in DompR. The binding of OmpR to these two sites was also demonstrated by DNA mobility shift assay. The possible mechanism underlying this positive regulation in Y. pseudotuberculosis is discussed. To our knowledge, this is the first report to demonstrate that OmpR positively regulates flhDC expression. INTRODUCTIONFlagella, the unique structure for motility, represent an important advantage for bacteria in moving towards favourable conditions or in avoiding detrimental environments. In pathogenic bacteria, flagella are usually considered as virulence factors (Josenhans & Suerbaum, 2002), and they play crucial roles in adhesion, colonization and biofilm formation of many bacteria such as Pseudomonas aeruginosa (Toutain et al., 2007), Escherichia coli (Pratt & Kolter, 1998), Vibrio cholerae (Gardel & Mekalanos, 1996) and Salmonella typhimurium (Ciacci-Woolwine et al., 1998). Flagellar gene regulation and assembly have been extensively characterized in E. coli and S. enterica serovar Typhimurium (Aldridge & Hughes, 2002). Over 60 genes, which are arranged into three classes (class I, class II and class III), are coordinately regulated and expressed in a transcriptional hierarchy (Chilcott & Hughes, 2000;Kanehisa et al., 2004;Kutsukake et al., 1990). Transcription of the downstream flagellar genes is dependent on a high expression level of some upstream genes. At the top of this hierarchy is the master operon composed of the genes flhD and flhC. FlhD and FlhC together form a heterohexameric transcriptional activator that binds to the class II operons (Wang et al., 2006). Due to the key role of flhDC in flagella synthesis, the regulation of its expression has been studied at both the transcriptional and post-transcriptional levels (Soutourina & Bertin, 2003). Many regulatory proteins, such as H-NS (Bertin et al., 1994;Soutourina et al., 1999), cAMP-CAP complex (catabolite gene activator protei...

show abstract

Section: Introductionmentioning

confidence: 99%

Positive regulation of flhDC expression by OmpR in Yersinia pseudotuberculosis

Wang

Ding

et al. 2009

Microbiology

View full text Add to dashboard Cite

show abstract

“…In E. coli, AI-2 stimulates biofilm formation and changes its architecture by stimulating flagellar motility via the quorumsensing regulator MqsR that acts through the two-component motility regulatory system QseBC (González Barrios et al, 2006), which transcriptionally regulates FlhDC, the master regulator of flagella and motility genes fliLMNOPQR, fliAZ, flhBA and flgABCDMN (Liu and Matsumura, 1994;Claret and Hughes, 2002;Clarke and Sperandio, 2005). This result is consistent with the recent finding that in the oral bacterium Aggregatibacter actinomycetemcomitans, AI-2 regulates its biofilm formation most likely through its QseBC system (Shao et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Escherichia coli transcription factor YncC (McbR) regulates colanic acid and biofilm formation by repressing expression of periplasmic protein YbiM (McbA)

2008

View full text Add to dashboard Cite

Quorum-sensing signal autoinducer 2 (AI-2) stimulates Escherichia coli biofilm formation through the motility regulator MqsR that induces expression of the putative transcription factor encoded by yncC. Here, we show that YncC increases biofilm formation by repressing overproduction of the exopolysaccharide identified as colanic acid (corroborated by decreasing mucoidy and increased sensitivity to bacteriophage P1 infection). Differential gene expression and gel shift assays demonstrated that YncC is a repressor of the predicted periplasmic protein-encoding gene, ybiM, which was corroborated by the isogenic yncC ybiM double mutation that repressed the yncC phenotypes (biofilm formation, colanic acid overproduction, mucoidy and bacteriophage resistance). Through nickel-enrichment DNA microarrays and additional gel shift assays, we found that the putative transcription factor B3023 (directly upstream of mqsR) binds the yncC promoter. Overexpressing MqsR, AI-2 import regulators LsrR/LsrK and AI-2 exporter TqsA induced yncC transcription, whereas the AI-2 synthase LuxS and B3023 repressed yncC. MqsR has a toxic effect on E. coli bacterial growth, which is partially reduced by the b3023 mutation. Therefore, AI-2 quorum-sensing control of biofilm formation is mediated through regulator MqsR that induces expression of the transcription factor YncC. YncC inhibits the expression of periplasmic YbiM, which prevents overproduction of colanic acid (excess colanic acid causes mucoidy) and prevents YbiM from inhibiting biofilm formation.

show abstract

“…Expression from the class 1 promoter is known to be controlled via a large number of global regulators, via unknown mechanisms (Clarke and Sperandio 2005;Ko and Park 2000;Teplitski et al 2003;Tomoyasu et al 2002;Wei et al 2001). It is also not clear how these inputs are integrated at the class 1 promoter (or posttranscriptionally) leading to the control of FlhD 4 C 2 production.…”

Section: Development Of the Mathematical Modelmentioning

confidence: 99%

Mathematical model of flagella gene expression dynamics in Salmonella enterica serovar typhimurium

et al. 2015

View full text Add to dashboard Cite

Flagellar assembly in Salmonella is controlled by an intricate genetic and biochemical network. This network comprises of a number of inter-connected feedback loops, which control the assembly process dynamically. Critical among these are the FliA-FlgM feedback, FliZ-mediated positive feedback, and FliT-mediated negative feedback. In this work, we develop a mathematical model to track the dynamics of flagellar gene expression in Salmonella. Analysis of our model demonstrates that the network is wired to not only control the transition of the cell from a non-flagellated to a flagellated state, but to also control dynamics of gene expression during cell division. Further, we predict that FliZ encoded in the flagellar regulon acts as a critical secretion-dependent molecular link between flagella and Salmonella Pathogenicity Island 1 gene expression. Sensitivity analysis of the model demonstrates that the flagellar regulatory network architecture is extremely robust to mutations.

show abstract

Transcriptional regulation of flhDC by QseBC and σ²⁸ (FliA) in enterohaemorrhagic Escherichia coli

Abstract: In the article by Clarke and Sperandio (2005) an error appeared in Fig. 1. The correct figure and legend are shown below.

Cited by 47 publications

References 3 publications

Positive regulation of flhDC expression by OmpR in Yersinia pseudotuberculosis

Positive regulation of flhDC expression by OmpR in Yersinia pseudotuberculosis

Escherichia coli transcription factor YncC (McbR) regulates colanic acid and biofilm formation by repressing expression of periplasmic protein YbiM (McbA)

Mathematical model of flagella gene expression dynamics in Salmonella enterica serovar typhimurium

Contact Info

Product

Resources

About