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Related Concept Videos

Gene Regulation in Microbial Communities: Quorum Sensing01:28

Gene Regulation in Microbial Communities: Quorum Sensing

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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Pathogenic bacteria employ a range of regulatory mechanisms to modulate the expression of virulence genes in response to environmental and host-derived signals. These mechanisms ensure that virulence factors are expressed only under favorable conditions, thereby optimizing infection and survival strategies.Mechanisms of Virulence RegulationKey regulatory strategies include:Two-Component Systems: These consist of a membrane-bound sensor kinase and a cytoplasmic response regulator. Environmental...
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Global regulatory systems in bacteria enable rapid and coordinated responses to environmental changes by integrating sensory inputs with gene expression, ensuring efficient adaptation to fluctuating conditions. Key global regulatory mechanisms include regulons, two-component systems, sigma factors, and secondary messengers.Regulons and Global RegulatorsA regulon is a collection of genes and operons controlled by a common global regulator. These regulators enable bacteria to prioritize resource...
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Quorum sensing in streptococci and its peptide-mediated modulation.

Bioscience reports·2026
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Mapping the Structural Determinants of Quorum Sensing Activity in <i>Streptococcus sinensis</i> Via Mutational Analysis of Its Competence Stimulating Peptide.

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The Quorum Sensing-Controlled Competence Regulon Drives H<sub>2</sub>O<sub>2</sub> Production in <i>Streptococcus gordonii</i>.

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Molecular Characterization of the Group A Streptococcus Virulence-Regulatory System FasBCAX.

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Deciphering the Regulatory Role and Molecular Interactions That Drive the Competence Regulon Quorum Sensing Circuitry in <i>Streptococcus constellatus</i>.

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Quantification of Violacein in Chromobacterium violaceum and Its Inhibition by Bioactive Compounds
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Development of Quorum Sensing Modulators of Streptococcus constellatus.

Keely M Rodriguez1, Daniel N Elliott1, Ella R Lemieux1

  • 1Department of Chemistry, University of Nevada, Reno, Reno, Nevada, USA.

Chembiochem : a European Journal of Chemical Biology
|June 30, 2026
PubMed
Summary

This study optimized a novel peptide analog, CSP-D1AI4AM6A, to inhibit quorum sensing (QS) in Streptococcus constellatus. This offers a new strategy to reduce the virulence of this opportunistic pathogen.

Keywords:
autoinducermicrobiologyquorum sensingrational designvirulence

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Drug Discovery

Background:

  • Streptococcus constellatus is an opportunistic pathogen causing severe infections.
  • Virulence factors, like genetic competence, are regulated by quorum sensing (QS).
  • QS in S. constellatus is mediated by a competence stimulating peptide (CSP).

Purpose of the Study:

  • To design and optimize novel QS inhibitors targeting CSP.
  • To develop competitive inhibitors for attenuating S. constellatus virulence.

Main Methods:

  • Rational design of second-generation peptide analog libraries.
  • Screening of analogs to identify potent QS inhibitors.
  • Determination of IC50 for optimized inhibitor CSP-D1AI4AM6A.

Main Results:

  • Identified target residues on CSP for mutation.
  • Optimized a competitive QS inhibitor, CSP-D1AI4AM6A.
  • Achieved a potent IC50 of 38.3 nM for CSP-D1AI4AM6A.

Conclusions:

  • Developed a rational framework for designing novel QS modulators.
  • CSP-D1AI4AM6A shows potential for attenuating S. constellatus virulence.
  • This approach can be applied to combat other opportunistic pathogens.