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Related Concept Videos

Gene Regulation in Microbial Communities: Quorum Sensing01:28

Gene Regulation in Microbial Communities: Quorum Sensing

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Quorum sensing is a mechanism of bacterial communication that enables coordinated gene expression in response to changes in population density. This facilitates collective behaviors that enhance survival, resource acquisition, and ecological adaptation. This process relies on small signaling molecules called autoinducers that accumulate as bacterial populations grow. When a critical threshold concentration of autoinducers is reached, bacterial cells collectively modify gene expression,...
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Bacterial signaling can occur within bacteria (intracellular) or between bacteria (intercellular). At times, a group of bacteria behaves like a community. To achieve this, they engage in quorum sensing, the perception of higher cell density that causes changes in gene expression. Quorum sensing involves both extracellular and intracellular signaling. The signaling cascade starts with a molecule called an autoinducer (AI). Individual bacteria produce AIs that move out of the bacterial cell...
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Antibiotic resistance is a major public health concern that arises when bacteria evolve mechanisms to withstand the effects of antibiotic treatments. This resistance can be intrinsic, acquired through genetic mutations, or transferred between bacteria via horizontal gene transfer. The development of antibiotic resistance poses significant challenges in treating bacterial infections and necessitates ongoing research to develop new therapeutic strategies.Intrinsic resistance occurs when bacterial...
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Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within...
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Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and...
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Related Experiment Video

Updated: Apr 11, 2026

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Why Antimicrobial Resistance Does Not Perpetually Expand in an Antibiotics-Free Environment: Insight from Quorum

Lin Zhu1,2, Mengdi Gao1, Jingpeng Li1

  • 1Zhejiang Key Laboratory of Solid Waste Pollution Control and Resource Utilization, School of Environmental Science and Engineering, Zhejiang Gongshang University, Hangzhou 310012, China.

Environmental Science & Technology
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Summary

Quorum sensing (QS) regulates antimicrobial resistance (AMR) in the environment. QS-deficient mutants reduce AMR, revealing a trade-off that limits resistance evolution without antibiotic pressure.

Keywords:
antibiotic resistancebiofilm tolerancelasR mutantquorum sensing policing

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Area of Science:

  • Microbiology
  • Evolutionary Biology
  • Environmental Science

Background:

  • Antimicrobial resistance (AMR) persists in environments without antibiotic pressure, posing a global health threat.
  • Mechanisms preventing unlimited AMR expansion in environments are poorly understood.
  • Quorum sensing (QS) is investigated for its role in constraining AMR.

Purpose of the Study:

  • To explore the role of quorum sensing (QS) in constraining antimicrobial resistance (AMR) under antibiotic-free conditions.
  • To understand the mechanisms behind the reversibility of environmental AMR.

Main Methods:

  • Long-term evolution experiments with antibiotic-resistant *Pseudomonas aeruginosa* strains.
  • Analysis of *las*R-deficient mutants (social cheaters) and their impact on AMR.
  • Investigation using reactive oxygen species scavengers to disrupt QS-mediated policing.

Main Results:

  • Spontaneous emergence of *las*R-deficient mutants (*Δlas*R) observed, acting as social cheaters.
  • *Δlas*R mutants showed reduced minimum inhibitory concentration and impaired biofilm formation, decreasing antibiotic-protected survival.
  • Increased *Δlas*R frequency correlated with decreased population-level resistance, accelerated by QS disruption.

Conclusions:

  • QS, specifically *las*R, plays a crucial role in maintaining AMR in environmental reservoirs.
  • An evolutionary trade-off favors *Δlas*R mutants in the absence of antibiotics, naturally selecting against resistance.
  • Targeting QS policing offers a potential strategy to mitigate environmental AMR.