The Fsr Quorum-Sensing System of Enterococcus faecalisModulates Surface Display of the Collagen-Binding MSCRAMM Ace through Regulation of gelE Original paper
Researched by:
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Divine Aleru
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Divine Aleru
Read MoreI am a biochemist with a deep curiosity for the human microbiome and how it shapes human health, and I enjoy making microbiome science more accessible through research and writing. With 2 years experience in microbiome research, I have curated microbiome studies, analyzed microbial signatures, and now focus on interventions as a Microbiome Signatures and Interventions Research Coordinator.
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Microbes
Microbes
Microbes are microscopic organisms living in and on the human body, shaping health through digestion, vitamin production, and immune protection. When microbial balance is disrupted, disease can occur. This guide explains key microbe types—bacteria, viruses, fungi, protozoa, and archaea—plus major pathogenic and beneficial examples.
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Divine Aleru
Read More
Researched by:
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Divine Aleru
ID
Divine Aleru
Read More
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Divine Aleru
What was studied?
This study examined the Fsr quorum-sensing system in Enterococcus faecalis and its role in regulating the surface display of the collagen-binding protein Ace, a key virulence factor. Researchers investigated how disruption of the Fsr system, as well as GelE protease activity, influenced the expression of Ace on the cell surface, its ability to adhere to collagen, and its overall contribution to virulence in infection models. The study used flow cytometry and ELISA to analyze Ace surface levels and protease activity.
Who was studied?
The study analyzed multiple Enterococcus faecalis strains, including the wild-type OG1RF and mutants lacking fsrB, gelE, or both. These strains were cultured and analyzed for their ability to display Ace, secrete GelE, and adhere to collagen in laboratory settings. The study also assessed the strains’ virulence in models of endocarditis and infection, focusing on the role of Ace and GelE in these processes.
What were the most important findings?
The study found that the Fsr quorum-sensing system regulates the surface display of Ace via the activity of the extracellular protease GelE. Disruption of the Fsr system or deletion of GelE resulted in prolonged display of Ace on the Enterococcus faecalis surface, especially during late growth phases, thereby enhancing collagen adhesion. GelE cleaved Ace from the cell surface, diminishing adhesion capabilities, particularly during stationary growth phases. The presence of GelE was crucial for the timing of Ace surface expression, and when GelE activity was inhibited (e.g., by EDTA), Ace levels remained high. These findings link quorum sensing with virulence factor modulation, providing insights into how E. faecalis adapts its adhesion profile to environmental conditions.
What are the greatest implications of this study?
This study highlights the complex regulation of virulence factors in Enterococcus faecalis, specifically how quorum-sensing mechanisms like the Fsr system can control the surface display of adhesion proteins like Ace. Understanding this regulatory process offers potential therapeutic strategies, such as targeting quorum sensing or GelE activity to prevent adhesion, biofilm formation, and infection progression, particularly in hospital-acquired infections.
Enterococcus faecalis
Enterococcus faecalis is a gut‑adapted, Gram‑positive, non‑spore‑forming facultative anaerobe that becomes an important opportunistic pathogen in healthcare when host barriers are breached or antibiotics select for enterococcal overgrowth. Its clinical impact is driven more by persistence, adhesion, and biofilm biology, quorum‑regulated secreted effectors (fsr‑controlled gelatinase GelE), and high genome plasticity than by a broad repertoire of classical tissue‑destroying toxins. Antimicrobial decision‑making must account for the intrinsic poor activity of cephalosporins, the potential for transferable glycopeptide resistance mediated by van gene clusters, and the need for regimen selection in endocarditis that respects synergy/tolerance and local high‑level aminoglycoside resistance patterns.