Effects of DNA supercoiling and topoisomerases on the expression of genes coding for F165<sub>1</sub>, a P-like fimbriae

Tessier, Marie-Catherine; Graveline, Richard; Crost, CÃ©cile; Desabrais, Julie Annick; Martin, Christine; Drolet, Marc; Harel, J

doi:10.1111/j.1574-6968.2007.00919.x

Cited by 8 publications

(9 citation statements)

References 26 publications

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“…Tessier et al (29) studied F165 adhesin from E. coli. This adhesin belongs to the family of Pap-related fimbriae, the expression of which is mediated by regulatory proteins such as Lrp, Dam-methylase, and FooI and FooB.…”

Section: Discussionmentioning

confidence: 99%

Effects of a Mutation in the gyrA Gene on the Virulence of Uropathogenic Escherichia coli

Sánchez‐Céspedes

Sáez-López

Frimodt‐Møller

et al. 2015

Antimicrob Agents Chemother

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dFluoroquinolones are among the drugs most extensively used for the treatment of bacterial infections in human and veterinary medicine. Resistance to quinolones can be chromosome or plasmid mediated. The chromosomal mechanism of resistance is associated with mutations in the DNA gyrase-and topoisomerase IV-encoding genes and mutations in regulatory genes affecting different efflux systems, among others. We studied the role of the acquisition of a mutation in the gyrA gene in the virulence and protein expression of uropathogenic Escherichia coli (UPEC). The HC14366M strain carrying a mutation in the gyrA gene (S83L) was found to lose the capacity to cause cystitis and pyelonephritis mainly due to a decrease in the expression of the fimA, papA, papB, and ompA genes. The levels of expression of the fimA, papB, and ompA genes were recovered on complementing the strain with a plasmid containing the gyrA wild-type gene. However, only a slight recovery was observed in the colonization of the bladder in the GyrA complement strain compared to the mutant strain in a murine model of ascending urinary tract infection. In conclusion, a mutation in the gyrA gene of uropathogenic E. coli reduced the virulence of the bacteria, likely in association with the effect of DNA supercoiling on the expression of several virulence factors and proteins, thereby decreasing their capacity to cause cystitis and pyelonephritis.

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Section: Discussionmentioning

confidence: 99%

Effects of a Mutation in the gyrA Gene on the Virulence of Uropathogenic Escherichia coli

Sánchez‐Céspedes

Sáez-López

Frimodt‐Møller

et al. 2015

Antimicrob Agents Chemother

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“…Moreover, flow cytometry data indicate that foo individual cells derived from an initial low level of fluorescence present two distinct populations, one with low fluorescence intensity and the second with partial intensity. This specific population suggests that the light blue colonies observed when the lacZ reporter system is under the control of the foo regulatory region result in a mixed population of white (OFF) and dark blue (ON) individual cells (16,27,28).…”

Section: Resultsmentioning

confidence: 99%

Monitoring F165 ₁ P-Like Fimbria Expression at the Single-Cell Level Reveals a Highly Heterogeneous Phenotype

et al. 2015

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A dherence to host cells relies on the synthesis of specialized molecules that play an important role in multiple steps during the infectious process. Adhesins contribute to virulence by promoting the attachment and bacterial colonization on the host cell surface. Escherichia coli possesses a wide variety of adhesins, which all differ in structure and in functions. Moreover, a single strain can present more than one adhesin. This implies a complex regulatory network to produce exclusively one adhesin or to simultaneously express more than one.Phase variation of P fimbriae is a stochastic and reversible switch between an on phenotype and an off phenotype, "all-ornothing" (ON/OFF), each capable of responding to a specific condition. After cell division, the majority of daughter cells retain the expression phase of the parent; a minority switches to the opposite expression phase. F165 1 fimbriae, encoded by the foo gene cluster, are members of the type P fimbria family of Escherichia coli (1-4). The regulatory region of foo shares more than 96% identity with that of the pyelonephritis-associated pili (pap) gene. Previous work showed that F165 1 fimbriae are essential for virulence and survival during systemic stages of infection in young pigs (5-8). F165 1 fimbriae are principally found in infections caused by opportunistic E. coli in animals, while Pap fimbriae are found in human clinical cases of urinary tract infections. The phase variation of F165 1 fimbriae shares similar features with that of the wellcharacterized Pap fimbriae (9-11). This includes an ϳ400-bp intergenic region surrounded by two divergently transcribed genes (papI and papB for Pap, fooI and fooB for F165 1 ). It also includes six leucine-responsive regulatory protein (Lrp) binding sites, of which two are GATC sites (referred to as GATC prox and GATC dist , respectively), spaced 102 bp apart. In pap and foo, phase variation occurs because of methylation-controlled modifications within the regulatory region of the fimbrial operon. This regulation is epigenetic since it does not involve any changes in DNA sequence (12). The differential methylation status of these sequences determines the binding of Lrp. Indeed, the switch from one phenotype to the other arises from the competition between the binding of Lrp at its distal or proximal binding sites and methylation by the Dam methyltransferase at the opposite GATC site (for reviews, see references 9, 10, and 11). When GATC dist is fully methylated, Lrp cooperatively binds to sites 1 to 3, maintaining the cells in the OFF state; when GATC prox is fully methylated, Lrp binds to sites 4 to 6, maintaining the ON state (Fig. 1). Control of pap expression also requires the action of PapI, a positive regulator that increases the affinity of Lrp for sites 4 to 6 in vivo (11,13). PapB, the second specific regulator of the pap operon, plays an important role by coordinating the expression of the pBA and pI promoters (11). All together, the combined actions of Lrp, Dam methyltransferase, PapI, and PapB result...

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“…Similarly, the mutation in topoI led to reduced expression of recA in E. coli, conferring increased UV sensitivity (Urios et al, 1990). Moreover, deletion of topoI reduced the expression of the fooB regulator required for the expression of fimbriae F165(1) needed for the virulence and pathogenesis of E. coli 4787 (O115 : KV165) (Tessier et al, 2007). Also, a mutation in topoI suppressed mutation of the leu-500 promoter (a supercoiling-sensitive promoter), leading to enhanced expression by perturbing the topology of regulatory DNA elements (Pruss & Drlica, 1985).…”

Section: Discussionmentioning

confidence: 99%

Reduction in DNA topoisomerase I level affects growth, phenotype and nucleoid architecture of Mycobacterium smegmatis

et al. 2015

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The steady-state negative supercoiling of eubacterial genomes is maintained by the action of DNA topoisomerases. Topoisomerase distribution varies in different species of mycobacteria. While Mycobacterium tuberculosis (Mtb) contains a single type I (TopoI) and a single type II (Gyrase) enzyme, Mycobacterium smegmatis (Msm) and other members harbour additional relaxases. TopoI is essential for Mtb survival. However, the necessity of TopoI or other relaxases in Msm has not been investigated. To recognize the importance of TopoI for growth, physiology and gene expression of Msm, we have developed a conditional knock-down strain of TopoI in Msm. The TopoI-depleted strain exhibited extremely slow growth and drastic changes in phenotypic characteristics. The cessation of growth indicates the essential requirement of the enzyme for the organism in spite of having additional DNA relaxation enzymes in the cell. Notably, the imbalance in TopoI level led to the altered expression of topology modulatory proteins, resulting in a diffused nucleoid architecture. Proteomic and transcript analysis of the mutant indicated reduced expression of the genes involved in central metabolic pathways and core DNA transaction processes. RNA polymerase (RNAP) distribution on the transcription units was affected in the TopoI-depleted cells, suggesting global alteration in transcription. The study thus highlights the essential requirement of TopoI in the maintenance of cellular phenotype, growth characteristics and gene expression in mycobacteria. A decrease in TopoI level led to altered RNAP occupancy and impaired transcription elongation, causing severe downstream effects.

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Effects of DNA supercoiling and topoisomerases on the expression of genes coding for F165₁, a P-like fimbriae

Cited by 8 publications

References 26 publications

Effects of a Mutation in the gyrA Gene on the Virulence of Uropathogenic Escherichia coli

Effects of a Mutation in the gyrA Gene on the Virulence of Uropathogenic Escherichia coli

Monitoring F165 ₁ P-Like Fimbria Expression at the Single-Cell Level Reveals a Highly Heterogeneous Phenotype

Reduction in DNA topoisomerase I level affects growth, phenotype and nucleoid architecture of Mycobacterium smegmatis

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Effects of DNA supercoiling and topoisomerases on the expression of genes coding for F1651, a P-like fimbriae

Cited by 8 publications

References 26 publications

Effects of a Mutation in the gyrA Gene on the Virulence of Uropathogenic Escherichia coli

Effects of a Mutation in the gyrA Gene on the Virulence of Uropathogenic Escherichia coli

Monitoring F165 1 P-Like Fimbria Expression at the Single-Cell Level Reveals a Highly Heterogeneous Phenotype

Reduction in DNA topoisomerase I level affects growth, phenotype and nucleoid architecture of Mycobacterium smegmatis

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Effects of DNA supercoiling and topoisomerases on the expression of genes coding for F165₁, a P-like fimbriae

Monitoring F165 ₁ P-Like Fimbria Expression at the Single-Cell Level Reveals a Highly Heterogeneous Phenotype