Use of the promoter fusion transposon Tn5 lac to identify mutations in Bordetella pertussis vir-regulated genes

Weiss, Alison A.; Melton, A R; Walker, Kimberly E.; Andraos-Selim, Cecile; Meidl, J J

doi:10.1128/iai.57.9.2674-2682.1989

Cited by 75 publications

(49 citation statements)

References 35 publications

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“…Bacterial strains and media. B. pertussis Tohama and its derivatives, BP338 (Bvg+) and BP347 (Bvg-), and the TnS lac transcription fusion strains used in this study were described previously (15,32). The TnS lac fusion in BPM409 (Bvg+) and BPM410 (Bvg-) is regulated by the fhaB promoter (32).…”

Section: Methodsmentioning

confidence: 99%

Characterization of environmental regulators of Bordetella pertussis

Melton

Weiss

1993

Infect Immun

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Bordetela pertussis suppresses transcription of its virulence genes in response to specific environmental conditions, a response called modulation. The organism responds to high concentrations of SO4 and C104 ions, nicotinic acid, and nicotinic acid analogs in vitro; however, the in vivo modulator has not been identified. We investigated which chemical structures of the nicotinic acid molecule are important for modulation by testing various analogs for their ability to modulate. The ring nitrogen of nicotinic acid was not required, since benzoic acid was a modulator. In contrast, the carboxyl group was required, since derivatives like ethylnicotinate, 3-pyridylcarbinol, 3-acetyl pyridine, and 6-chloronicotinamide with altered carboxyl groups were not modulators. The planar ring structure or resonance in the ring was required for modulation, since nipecotic acid failed to modulate. The most potent modulators were nicotinic acid derivatives with electron-withdrawing substituents in the meta orpara position relative to the carboxyl group. Relative hydrophilicity of substituents did not appear to contribute to modulation. Although these modulators elicited a clear biological response, the mechanism of modulation remains unclear, because no binding of the modulator 3 So4 or [14C]4-chlorobenzoic acid to whole B. pertussis was detected. However, modulation appears to involve a charge-charge interaction, since the response was blocked by chlorine ions.

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Section: Methodsmentioning

confidence: 99%

Characterization of environmental regulators of Bordetella pertussis

Melton

Weiss

1993

Infect Immun

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“…See Table 1 for strain description. phenotypically FHA minus [11,12] were both serum resistant (Fig. 1).…”

Section: Role Of Fha In Serum Resistancementioning

confidence: 96%

“…1). Strain BPM409, which has a transposon insertion in the structural gene for FHA [12] appears to be less resistant to killing (Fig. 1), but this was not statistically signi¢cant (P 6 0.051) when compared to wild-type B. pertussis.…”

Section: Role Of Fha In Serum Resistancementioning

confidence: 96%

Serum resistance in bvg-regulated mutants of Bordetella pertussis

Fernandez¹

1998

FEMS Microbiology Letters

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Serum resistance, or resistance to killing by antibody dependent pathway of complement, in Bordetella pertussis is bvgregulated and the Bordetella resistance to killing (brk) locus mediates much of the resistance. Here we examined whether other bvg-regulated proteins contribute to serum resistance. We found that neither pertussis toxin, adenylate cyclase toxin, filamentous hemagglutinin, dermonecrotic toxin, tracheal colonization factor, nor Vag8 mutants were sensitive to serum killing compared to the wild-type. Filamentous hemagglutinin has been reported to bind C4 binding protein, an inhibitor of complement, but this activity does not appear to contribute to serum resistance, as evidenced by the resistant phenotype of FHA mutants. Clinical isolates were serum resistant and wild-type strains possessing an additional copy of the brk locus were 2^5-fold more resistant to serum killing. z

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“…Bordetella pertussis, the etiologic agent of the severe respiratory disease whooping cough, expresses an array of virulence factors that contribute to its ability to cause disease (13,14,34,46,48). These factors include cell surface proteins that are thought to be involved in the adherence of the organism to ciliated respiratory epithelial cells, as well as several extracellular toxins that inhibit host defenses and induce damage to host tissues.…”

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confidence: 99%

Contribution of Regulation by the bvgLocus to Respiratory Infection of Mice by Bordetella pertussis

et al. 1998

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Whooping cough is an acute respiratory disease caused by the small, gram-negative bacterium Bordetella pertussis. B. pertussis expresses several factors that contribute to its ability to cause disease. These factors include surface-associated molecules, which are involved in the adherence of the organism to respiratory epithelial cells, as well as several extracellular toxins that inhibit host defenses and induce damage to host tissues. The expression of virulence factors in B. pertussis is dependent upon the bvg locus, which consists of three genes: bvgA, bvgS, and bvgR. The bvgAS genes encode a two-component regulatory system consisting of a sensor protein, BvgS, and a transcriptional activator, BvgA. Upon modification by BvgS, BvgA binds to the promoter regions of the bvg-activated genes and activates transcription. One of the bvg-activated genes, bvgR, is responsible for the regulation of the bvg-repressed genes, the functions of which are unknown. The fact that these genes are regulated by the bvg locus suggests that they play a role in the pathogenesis of the bacterium. In order to evaluate the contribution of bvg-mediated regulation to the virulence of B. pertussis and determine if expression of the bvg-repressed genes is required for the virulence of B. pertussis, we examined the ability of B. pertussis mutants, defective in their ability to regulate the expression of the bvg-activated and/or the bvg-repressed genes, to cause disease in the mouse aerosol challenge model. Our results indicate that the bvgR-mediated regulation of gene expression contributes to respiratory infection of mice.

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Use of the promoter fusion transposon Tn5 lac to identify mutations in Bordetella pertussis vir-regulated genes

Cited by 75 publications

References 35 publications

Characterization of environmental regulators of Bordetella pertussis

Characterization of environmental regulators of Bordetella pertussis

Serum resistance in bvg-regulated mutants of Bordetella pertussis

Contribution of Regulation by the bvgLocus to Respiratory Infection of Mice by Bordetella pertussis

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