Pheromone-inducible conjugation in Enterococcus faecalis: interbacterial and host-parasite chemical communication

Dunny, Gary M.; Leonard, Bettina A. B.; Hedberg, P. J.

doi:10.1128/jb.177.4.871-876.1995

Cited by 155 publications

(107 citation statements)

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“…E. faecalis strains carry a variety of mobile genetic elements, including conjugative transposons and plasmids that encode antibiotic resistance, haemolysins or other virulence factors. They are also known to secrete a number of small, hydrophobic peptide pheromones, and a family of conjugative plasmids has evolved to allow the host to sense the presence of just one of the pheromone types and initiate a mating response (reviewed in Dunny et al, 1995). Transfer of the conjugative plasmid pCF10 from donor strains is induced by the peptide pheromone cCF10, which is secreted by potential recipient cells (cells not carrying pCF10).…”

Section: Introductionmentioning

confidence: 99%

Pheromone cCF10 and plasmid pCF10‐encoded regulatory molecules act post‐transcriptionally to activate expression of downstream conjugation functions

Bensing

Manias

Dunny

1997

Molecular Microbiology

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SummaryExpression of aggregation protein Asc10 from the prgB gene of conjugative plasmid pCF10 in Enterococcus faecalis is induced by the peptide pheromone cCF10. Genes required for Asc10 production, prgQ and prgS, lie 3-5 kb upstream, but can function at much greater distances. The prgQ transcripts encode a pheromone inhibitor peptide (iCF10) at the extreme 5Ј end. Neither production of this peptide nor translation of the 5Ј end of prgQ transcripts was found to be necessary for prgB expression. Pheromone cCF10 is required to activate prgB expression, even in the absence of iCF10 production, and does not affect initiation of transcription. The prgS gene encodes a 10.5 kDa protein that appears to be required for translation of prgB, and a non-coding RNA at the 3Ј end of prgS may be required for readthrough of transcription to prgB from the prgQ promoter. Although the entire positive control region is transcribed constitutively from the prgQ promoter, translation of PrgS and transcriptional readthrough to prgB occur only after induction with pheromone. The combined data are consistent with a model in which the positive regulatory molecules and pheromone cCF10 activate prgB expression post-transcriptionally.

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Section: Introductionmentioning

confidence: 99%

Pheromone cCF10 and plasmid pCF10‐encoded regulatory molecules act post‐transcriptionally to activate expression of downstream conjugation functions

Bensing

Manias

Dunny

1997

Molecular Microbiology

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“…The prgQ gene encodes a 23-aa polypeptide that is cleaved to a 7-aa peptide, iCF10, which can inhibit the action of pheromone (7). However, the functionalprgQ gene product required for activation of AsclO expression is a 530-nt RNA molecule, QL, that encodes the inhibitor peptide at its extreme 5' end (8,9). The second essential positive control gene,prgS, encodes a 10.5-kDa basic protein that shows no significant similarity to proteins reported in the Protein Information Resource or GenBank databases (10).…”

mentioning

confidence: 99%

Sensitive detection of bacterial transcription initiation sites and differentiation from RNA processing sites in the pheromone-induced plasmid transfer system of Enterococcus faecalis.

Bensing

Meyer

Dunny

1996

Proc. Natl. Acad. Sci. U.S.A.

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A method was developed to detect 5' ends of bacterial RNAs expressed at low levels and to differentiate newly initiated transcripts from processed transcripts produced in vivo. The procedure involves use of RNA ligase to link a specific oligoribonucleotide to the 5' ends of cellular RNAs, followed by production of cDNA and amplification of the gene of interest by PCR. The method was used to identify the precise sites of transcription initiation within a 10-kb region of the pheromone-inducible conjugative plasmid pCF10 of Enterococcus faecalis. Results confirmed the 5' end of a very abundant, constitutively produced transcript (fromprgQ) that had been mapped previously by primer extension and defined the initiation point of a less abundant, divergently transcribed message (from prgX). The method also showed that the 5' end of a pheromone-inducible transcript (prgB) that had been mapped by primer extension was generated by processing rather than new initiation. In addition, the results provided evidence for two promoters, 3 and 5 kb upstream ofprgB, and indicated that only the transcripts originating 5 kb upstream may be capable of extending to prgB.

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“…6 An additional challenge to treating infections with these organisms is their intrinsic resistance to several classes of antimicrobial agents, including cephalosporins and aminoglycosides, and their ability to accumulate additional resistance genes through plasmid transfer. 7 It is the accumulation of the van genes, which code for enzymes that alter the vancomycin binding target on the bacterial cell wall, that allows enterococci to become resistant to vancomycin.…”

mentioning

confidence: 99%

Rising Vancomycin-Resistant Enterococcus Infections in Hospitalized Children in the United States

Adams

Eberly

Goudie

et al. 2016

Hospital Pediatrics

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A B S T R A C T OBJECTIVE:Vancomycin-resistant Enterococcus (VRE) is an emerging drug-resistant organism responsible for increasing numbers of nosocomial infections in adults. Few data are available on the epidemiology and impact of VRE infections in children. We hypothesized a significant increase in VRE infections among hospitalized children. Additionally, we predicted that VRE infection would be associated with certain comorbid conditions and increased duration and cost of hospitalization. METHODS:A retrospective study of inpatient pediatric patients was performed using data on hospitalizations for VRE from the Healthcare Cost and Utilization Project Kids' Inpatient Database from 1997 to 2012. We used a multivariable logistic regression model to establish factors associated with VRE infection and a high-dimensional propensity score match to evaluate death, length of stay, and cost of hospitalization. RESULTS: Hospitalizations for VRE infection showed an increasing trend, from 53 hospitalizationsper million in 1997 to 120 in 2012 (P , .001). Conditions associated with VRE included Clostridium difficile infection and other diagnoses involving immunosuppression and significant antibiotic and health care exposure. Patients with VRE infection had a significantly longer length of stay (attributable difference [AD] 2.1 days, P , .001) and higher hospitalization costs (AD $8233, P 5 .004). VRE infection was not associated with an increased risk of death (odds ratio 1.03; 95% confidence interval 0.73-1.47).CONCLUSIONS: VRE infections among hospitalized children are increasing at a substantial rate. This study demonstrates the significant impact of VRE on the health of pediatric patients and highlights the importance of strict adherence to existing infection control policies and VRE surveillance in certain high-risk pediatric populations.

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Pheromone-inducible conjugation in Enterococcus faecalis: interbacterial and host-parasite chemical communication

Cited by 155 publications

References 64 publications

Pheromone cCF10 and plasmid pCF10‐encoded regulatory molecules act post‐transcriptionally to activate expression of downstream conjugation functions

Pheromone cCF10 and plasmid pCF10‐encoded regulatory molecules act post‐transcriptionally to activate expression of downstream conjugation functions

Sensitive detection of bacterial transcription initiation sites and differentiation from RNA processing sites in the pheromone-induced plasmid transfer system of Enterococcus faecalis.

Rising Vancomycin-Resistant Enterococcus Infections in Hospitalized Children in the United States

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