The yicJI metabolic operon of Escherichia coli is involved in bacterial fitness

Répérant, Maryline; Porcheron, Gaëlle; Rouquet, Géraldine; Gilot, Philippe

doi:10.1111/j.1574-6968.2011.02281.x

Cited by 7 publications

(3 citation statements)

References 23 publications

(29 reference statements)

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“…The papC gene percentage was 10% (1/10), which indicates that a low pathogenic strain of APEC was responsible for the septicemia that infected many organs later on in the infectious process (38). In, contrast prior research showed that 33.33 % of the papC gene was found in E. coli isolates, which was higher than the average (39).…”

Section: Discussioncontrasting

confidence: 59%

Isolation and molecular detection of some virulence associated genes in avian pathogenic E. coli

Hasan¹,

Abdulla²,

Ulaiwi³

2022

IJVS

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There are 13 virulence-related genes in E. coli isolates. The10 genes of these isolates were selected from avian pathogenic E. coli in some Iraqi broiler farms. Six of these virulence-related genes (iroN, iucC, frz operon, iucD, papC, and R4) were investigated in these isolates by PCR. Eighty percent of the isolates had one or more virulence-associated genes. Two APEC separates carried just one gene, iroN or iucC. According to preliminary evidence, the iroN and iucC genes may express their pathogenicity independently. All of the strains had the same iroN gene, making them all pathogenic. The results of these isolates were confirmed by PCR to have the six pathogenic genes: 80% positive for iucC, 50% positive for iucD, 100% positive for iroN, 10% positive for frz operon, 10% positive for papC, and 0% positive for R4 respectively. These six virulence genes were detected with different percentages in isolates; the iroN gene was found in all isolates but the other virulence genes were found with different percentages in E. coli isolates. According to, detection the iroN and such genes are displaying their pathogenicity separately from each other.

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Section: Discussioncontrasting

confidence: 59%

Isolation and molecular detection of some virulence associated genes in avian pathogenic E. coli

Hasan¹,

Abdulla²,

Ulaiwi³

2022

IJVS

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“…T6SS2 location is conserved in most of STEC including EHEC O157:H7 strain, suggesting that the transfer event has not occur recently. On the other hand, T6SS1 is inserted in STEC O22:H8 (154) close to tRNA SelC inside of yicIJH operon, which is involved in sugars efflux 28 (Supplementary Figure 3B). The yicIJH operon is part of the common genetic backbone in most of the E. coli , including symbionts and pathogenic strains 27 .…”

Section: Resultsmentioning

confidence: 99%

Antibacterial T6SS1 cluster identification and bioinformatics characterization of their putative effectors in Shiga toxin-producingEscherichia coli

Riviere,

Casabonne,

Smith

et al. 2024

Preprint

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Shiga toxing-producing Escherichia coli (STEC) O22:H8 strain is a serotype occasionally isolated in Argentinian cattle. Preliminary works showed that the cattle carrying STEC O22:H8 strains could not be experimentally colonized by EHEC O157:H7 strain. The type 6 secretion system (T6SS) is one of the most versatile virulence mechanisms involved in delivering effectors, particularly the T6SS1 translocate antibacterial toxins effectors during bacterial competition for niche-space. In this work, we could evidence the molecular bases of the success of STEC O22:H8 (154) strain during bacterial competition against EHEC O157:H7 strains. The genome sequence of STEC O22:H8 (154) allowed us to identify a complete T6SS1 cluster. In addition, we identify and characterized several putative T6SS1-antibacterial effectors encoded inside the T6SS1 clusters and in genomic pathogenic islands. Competition assays against EHEC O157:H7 strain confirmed the antibacterial activity of STEC O22:H8 (154) strain in vitro. Considering the absent of T6SS1 in STEC strains, we proposed the recent horizontal transfer acquisition and the most probably donor belong to the same Escherichia coli species. A safe STEC O22:H8 (154) Δstx would be used as a new strategy to fight STECs in bovine intestinal colonization, leading in a reduction in beef contamination and consequently HUS cases in humans.

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“…The arabinose operon regulatory protein activates the transcription of the araBAD operon, which has been well studied in Escherichia coli as a regulatory system for cellular response to environmental changes [ 27 ]. The symporter YicJ is associated with bacterial fitness (resistance to heat shock) and increase in growth rate in E. coli [ 28 , 29 ]. LysR family transcriptional regulators are involved in virulence regulation in Salmonella [ 30 ].…”

Section: Resultsmentioning

confidence: 99%

Emergence of Resistance Mutations in Salmonella enterica Serovar Typhi Against Fluoroquinolones

Matono

Morita

Yahara

et al. 2017

Open Forum Infectious Diseases

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BackgroundLittle is known about the evolutionary process and emergence time of resistance mutations to fluoroquinolone in Salmonella enterica serovar Typhi.MethodsWe analyzed S. Typhi isolates collected from returned travelers between 2001 and 2016. Based on ciprofloxacin susceptibility, isolates were categorized as highly resistant (minimum inhibitory concentration [MIC] ≥ 4 μg/mL [CIPHR]), resistant (MIC = 1–2 μg/mL [CIPR]), intermediate susceptible (MIC = 0.12–0.5 μg/mL [CIPI]), and susceptible (MIC ≤ 0.06 μg/mL [CIPS]).ResultsA total of 107 isolates (33 CIPHR, 14 CIPR, 30 CIPI, and 30 CIPS) were analyzed by whole-genome sequencing; 2461 single nucleotide polymorphisms (SNPs) were identified. CIPS had no mutations in the gyrA or parC genes, while each CIPI had 1 of 3 single mutations in gyrA (encoding Ser83Phe [63.3%], Ser83Tyr [33.3%], or Asp87Asn [3.3%]). CIPHR had the same 3 mutations: 2 SNPs in gyrA (encoding Ser83Phe and Asp87Asn) and a third in parC (encoding Ser80Ile). CIPHR shared a common ancestor with CIPR and CIPI isolates harboring a single mutation in gyrA encoding Ser83Phe, suggesting that CIPHR emerged 16 to 23 years ago.ConclusionsThree SNPs—2 in gyrA and 1 in parC—are present in S. Typhi strains highly resistant to fluoroquinolone, which were found to have evolved in 1993–2000, approximately 10 years after the beginning of the ciprofloxacin era. Highly resistant strains with survival advantages arose from strains harboring a single mutation in gyrA encoding Ser83Phe. Judicious use of fluoroquinolones is warranted to prevent acceleration of such resistance mechanisms in the future.

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The yicJI metabolic operon of Escherichia coli is involved in bacterial fitness

Cited by 7 publications

References 23 publications

Isolation and molecular detection of some virulence associated genes in avian pathogenic E. coli

Isolation and molecular detection of some virulence associated genes in avian pathogenic E. coli

Antibacterial T6SS1 cluster identification and bioinformatics characterization of their putative effectors in Shiga toxin-producingEscherichia coli

Emergence of Resistance Mutations in Salmonella enterica Serovar Typhi Against Fluoroquinolones

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