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Antagonistic Donor Density Effect Conserved in Multiple Enterococcal Conjugative Plasmids. | LitMetric

Antagonistic Donor Density Effect Conserved in Multiple Enterococcal Conjugative Plasmids.

Appl Environ Microbiol

Department of Chemical Engineering and Materials Science, University of Minnesota, Minneapolis, Minnesota, USA

Published: August 2016

AI Article Synopsis

  • Enterococcus faecalis is a major cause of hospital infections and is resistant to many antibiotics, raising public health concerns due to its ability to share resistance genes through conjugative plasmids.
  • Recent research found that the plasmid pCF10 utilizes a quorum-sensing system where an inhibitor peptide reduces the response to pheromones, impacting the transfer of plasmids.
  • Similar studies on plasmids pAD1 and pAM373 suggest that higher donor cell densities lead to reduced conjugation rates, indicating that these plasmids may share regulatory behaviors.

Article Abstract

Unlabelled: Enterococcus faecalis, a common causative agent of hospital-acquired infections, is resistant to many known antibiotics. Its ability to acquire and transfer resistance genes and virulence determinants through conjugative plasmids poses a serious concern for public health. In some cases, induction of transfer of E. faecalis plasmids results from peptide pheromones produced by plasmid-free recipient cells, which are sensed by the plasmid-bearing donor cells. These plasmids generally encode an inhibitory peptide that competes with the pheromone and suppresses self-induction of donors. We recently demonstrated that the inhibitor peptide encoded on plasmid pCF10 is part of a unique quorum-sensing system in which it functions as a "self-sensing signal," reducing the response to the pheromone in a density-dependent fashion. Based on the similarities between regulatory features controlling conjugation in pAD1 and pAM373 and those controlling conjugation in pCF10, we hypothesized that these plasmids are likely to exhibit similar quorum-sensing behaviors. Experimental findings indicate that for both pAD1 and pAM373, high donor densities indeed resulted in decreased induction of the conjugation operon and reduced conjugation frequencies. This effect was restored by the addition of exogenous inhibitor, confirming that the inhibitor serves as an indicator for donor density. Donor density also affects cross-species conjugative plasmid transfer. Based on our experimental results, we propose models for induction and shutdown of the conjugation operon in pAD1 and pAM373.

Importance: Enterococcus faecalis is a leading cause of hospital-acquired infections. Its ability to transfer antibiotic resistance and virulence determinants by sharing its genetic material with other bacteria through direct cell-cell contact via conjugation poses a serious threat. Two antagonistic signaling peptides control the transfer of plasmids pAD1 and pAM373: a peptide pheromone produced by plasmid-free recipients triggers the conjugative transfer in plasmid-containing donors, and an inhibitor peptide encoded on the plasmid and produced by donor cells serves to modulate the donor response in accordance with the relative abundance of donors and recipients. We demonstrate that high donor density reduces the conjugation frequency of both of these plasmids, which is a consequence of increased inhibitor concentration in high-donor-density cultures. While most antibiotic strategies end up selecting resistant strains and disrupting the community balance, manipulating bacterial signaling mechanisms can serve as an alternate strategy to prevent the spread of antibiotic resistance.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4984291PMC
http://dx.doi.org/10.1128/AEM.00363-16DOI Listing

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