Environmental regulation of the fim switch controlling type 1 fimbrial phase variation in Escherichia coli K-12: effects of temperature and media

Gally, David L.; Bogan, Jacqueline A; Eisenstein, Barry I.; Blomfield, Ian C.

doi:10.1128/jb.175.19.6186-6193.1993

Cited by 203 publications

(271 citation statements)

References 42 publications

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“…FimBpromoted recombination was measured using a minimal MOPS XGal plating assay, essentially as described previously (Gally et al, 1993;Holden et al, 2001). In brief, for off-to-on recombination frequencies, a white colony was selected, diluted in PBS to a suitable cell number, and plated onto minimal MOPS X-Gal agar.…”

Section: Methodsmentioning

confidence: 99%

Demonstration of regulatory cross-talk between P fimbriae and type 1 fimbriae in uropathogenic Escherichia coli

et al. 2006

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The majority of Escherichia coli strains isolated from urinary tract infections have the potential to express multiple fimbriae. Two of the most common fimbrial adhesins are type 1 fimbriae and pyelonephritis-associated pili (Pap). Previous research has shown that induced, plasmid-based expression of a Pap regulator, papB, and its close homologues can prevent inversion of the fim switch controlling the expression of type 1 fimbriae. The aim of the present study was to determine if this cross-regulation occurs when PapB is expressed from its native promoter in the chromosome of E. coli K-12 and clinical isolates. The regulation was examined in three ways: (1) mutated alleles of the pap regulatory region, including papB and papI, that maintain the pap promoter in either the off or the on phase were exchanged into the chromosome of both E. coli K-12 and the clinical isolate E. coli CFT073, and the effect on type 1 fimbrial expression was measured; (2) type 1 fimbrial expression was determined using a novel fimS : : gfp + reporter system in mutants of the clinical isolate E. coli 536 in which combinations of complete fimbrial clusters had been deleted; (3) type 1 fimbrial expression was determined in a range of clinical isolates and compared with both the number of P clusters and their expression. All three approaches demonstrated that P expression represses type 1 fimbrial expression. Using a number of novel genetic approaches, this work extends the initial finding that PapB inhibits FimB recombination to the impact of this regulation in clinical isolates. INTRODUCTIONUrinary tract infections (UTIs) are common, affecting a large proportion of the population. It is estimated that 20 % of women develop a UTI in their lifetime, and antibiotic treatment results in approximately 110 000 prescriptions per million inhabitants per annum in Europe (Naber, 2000). Escherichia coli strains are the predominant cause of uncomplicated UTIs, responsible for between 60 and 80 % of the cases reported in the UK each year (Graham & Galloway, 2001). Many infections are asymptomatic, especially in the elderly (Nicolle, 2001), but others result in cystitis. If the infection ascends to the kidney, then pyelonephritis can occur. Such infections are a significant origin of Gramnegative sepsis.Fimbrial adhesins are important virulence factors that allow binding of the bacteria to specific receptors on epithelial cells of the urinary tract. The two adhesins most commonly associated with UTI are type 1 fimbriae, and pyelonephritisassociated pili (Pap) and Pap-related fimbriae (Prf); the last two are collectively termed P fimbriae in this study. Type 1 fimbriae mediate binding to a-D-mannose-containing receptors and extracellular matrix components, whereas P fimbriae bind to glycoreceptors containing the aGal(1-4)bGal moiety (Lindberg et al., 1984). Although type 1 fimbriae are common to the majority of E. coli isolates, the FimH adhesin has been shown to be important in a mouse model of UTI, and a degranulation response to the fimbriae is asso...

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Section: Methodsmentioning

confidence: 99%

Demonstration of regulatory cross-talk between P fimbriae and type 1 fimbriae in uropathogenic Escherichia coli

et al. 2006

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“…The fim system in uropathogenic strains of the bacterium E. coli controls the production of Type 1 fimbriae (or pili), which are "hairs" on the surface of the bacterium. Individual cells switch stochastically between "on" and "off" states of fimbrial production [1,26,27,28]. The key feature of the fim switch is a short piece of DNA that can be inserted into the bacterial DNA in two possible orientations.…”

Section: Introductionmentioning

confidence: 99%

Statistical physics of a model binary genetic switch with linear feedback

Visco

Allen²,

Evans³

2009

Phys. Rev. E

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We study the statistical properties of a simple genetic regulatory network that provides heterogeneity within a population of cells. This network consists of a binary genetic switch in which stochastic flipping between the two switch states is mediated by a "flipping" enzyme. Feedback between the switch state and the flipping rate is provided by a linear feedback mechanism: the flipping enzyme is only produced in the on switch state and the switching rate depends linearly on the copy number of the enzyme. This work generalises the model of [Phys. Rev. Lett., 101, 118104] to a broader class of linear feedback systems. We present a complete analytical solution for the steady-state statistics of the number of enzyme molecules in the on and off states, for the general case where the enzyme can mediate flipping in either direction. For this general case we also solve for the flip time distribution, making a connection to first passage and persistence problems in statistical physics. We show that the statistics of the model are non-Poissonian, leading to a peak in the flip time distribution. The occurrence of such a peak is analysed as a function of the parameter space. We present a new relation between the flip time distributions measured for two relevant choices of initial condition. We also introduce a new correlation measure to show that this model can exhibit long-lived temporal correlations, thus providing a primitive form of cellular memory. Motivated by DNA replication as well as by evolutionary mechanisms involving gene duplication, we study the case of two switches in the same cell. This results in correlations between the two switches; these can either positive or negative depending on the parameter regime.

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“…5a). In contrast, other studies inactivated fimE with an IS1 insertion sequence 31,33 and the exact sequence changes were not reported. It is possible that the latter method deleted flanking sequences that influence fimS inversion bias.…”

Section: Resultsmentioning

confidence: 75%

“…Previous studies found little-to-no bias in FimB inversion [31][32][33] . One explanation for the difference is that when we replaced both fimB and fimE genes with Kan R , the distal 230 bp of fimE was left intact to minimize effects that the sequence replacement might have on inversion of the neighbouring fimS (HL4366, Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The orientation of fimS is controlled by the FimB and FimE recombinases. FimB reportedly switches fimS in both directions at approximately equal rates (10 À 2 -10 À 3 cells Á generation À 1 ) in the absence of FimE [31][32][33] and thus, FimB controls the frequency of the transitions. FimE only inverts fimS from ON to OFF and thus it affects the bias.…”

Section: Resultsmentioning

confidence: 99%

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Modulating the frequency and bias of stochastic switching to control phenotypic variation

et al. 2014

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Mechanisms that control cell-to-cell variation in gene expression ('phenotypic variation') can determine a population's growth rate, robustness, adaptability and capacity for complex behaviours. Here we describe a general strategy (termed FABMOS) for tuning the phenotypic variation and mean expression of cell populations by modulating the frequency and bias of stochastic transitions between 'OFF' and 'ON' expression states of a genetic switch. We validated the strategy experimentally using a synthetic fim switch in Escherichia coli. Modulating the frequency of switching can generate a bimodal (low frequency) or a unimodal (high frequency) population distribution with the same mean expression. Modulating the bias as well as the frequency of switching can generate a spectrum of bimodal and unimodal distributions with the same mean expression. This remarkable control over phenotypic variation, which cannot be easily achieved with standard gene regulatory mechanisms, has many potential applications for synthetic biology, engineered microbial ecosystems and experimental evolution.

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Environmental regulation of the fim switch controlling type 1 fimbrial phase variation in Escherichia coli K-12: effects of temperature and media

Cited by 203 publications

References 42 publications

Demonstration of regulatory cross-talk between P fimbriae and type 1 fimbriae in uropathogenic Escherichia coli

Demonstration of regulatory cross-talk between P fimbriae and type 1 fimbriae in uropathogenic Escherichia coli

Statistical physics of a model binary genetic switch with linear feedback

Modulating the frequency and bias of stochastic switching to control phenotypic variation

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