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Updated: May 12, 2026

Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection
Published on: October 25, 2013
Antagonistic self-sensing and mate-sensing signaling controls antibiotic-resistance transfer
Anushree Chatterjee1, Laura C C Cook, Che-Chi Shu
1Department of Chemical Engineering and Materials Science, University of Minnesota, Minneapolis, MN 55455, USA.
Abstract:
Conjugation is one of the most common ways bacteria acquire antibiotic resistance, contributing to the emergence of multidrug-resistant "superbugs." Bacteria of the genus Enterococcus faecalis are highly antibiotic-resistant nosocomial pathogens that use the mechanism of conjugation to spread antibiotic resistance between resistance-bearing donor cells and resistance-deficient recipient cells. Here, we report a unique quorum sensing-based communication system that uses two antagonistic signaling molecules to regulate conjugative transfer of tetracycline-resistance plasmid pCF10 in E. faecalis. A "mate-sensing" peptide sex pheromone produced by recipient cells is detected by donor cells to induce conjugative genetic transfer. Using mathematical modeling and experimentation, we show that a second antagonistic "self-sensing" signaling peptide, previously known to suppress self-induction of donor cells, also serves as a classic quorum-sensing signal for donors that functions to reduce antibiotic-resistance transfer at high donor density. This unique form of quorum sensing may provide a means of limiting the spread of the plasmid and present opportunities to control antibiotic-resistance transfer through manipulation of intercellular signaling, with implications in the clinical setting.
Insights
Bacteria use conjugation to spread antibiotic resistance, creating superbugs. This study reveals a novel communication system in Enterococcus faecalis that uses two signals to control the spread of tetracycline resistance, offering potential clinical control strategies.
Area of Science:
- Microbiology
- Bacterial genetics
- Molecular biology
Background:
- Conjugation is a primary mechanism for bacterial antibiotic resistance acquisition.
- Enterococcus faecalis is a significant nosocomial pathogen known for antibiotic resistance.
- Plasmid transfer via conjugation facilitates the rapid spread of resistance genes.
Purpose of the Study:
- To investigate the regulatory mechanisms of conjugative plasmid transfer in Enterococcus faecalis.
- To elucidate the role of quorum sensing in controlling the spread of tetracycline resistance.
- To identify potential targets for controlling antibiotic resistance transfer.
Main Methods:
- Mathematical modeling of bacterial communication systems.
- Experimental analysis of gene transfer dynamics.
- Identification and characterization of signaling peptides involved in conjugation.
Main Results:
- A unique quorum sensing system regulates the conjugative transfer of the tetracycline-resistance plasmid pCF10.
- Two antagonistic signaling peptides control plasmid transfer based on cell density.
- A 'self-sensing' peptide suppresses transfer at high donor cell densities.
Conclusions:
- The identified quorum sensing system provides a novel mechanism for limiting plasmid spread.
- Manipulation of these signaling pathways could offer strategies to combat antibiotic resistance.
- Understanding intercellular communication is crucial for controlling the emergence of multidrug-resistant bacteria.
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