ArticleInfection and immunity2005
Fsr-independent production of protease(s) may explain the lack of attenuation of an Enterococcus faecalis fsr mutant versus a gelE-sprE mutant in induction of endocarditis.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis.Nature communications · 2026Article
- Insights into ecology, pathogenesis, and biofilm formation ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Role of theApplied and environmental microbiology · 2022Article
- Article
- The gelatinase biosynthesis-activating pheromone binds and stabilises the FsrB membrane protein in Enterococcus faecalis quorum sensing.FEBS letters · 2020Article
- N-Methylation of Amino Acids in Gelatinase Biosynthesis-Activating Pheromone Identifies Key Site for Stability Enhancement with Retention of the Enterococcus faecalis fsr Quorum Sensing Circuit Response.ACS infectious diseases · 2019Article
- Evaluation of the Effect of MTAD on Expression of Enterococcus faecalis Virulence Factors Considering the Role of Different Obturating Materials.Journal of dentistry (Tehran, Iran) · 2018Article
- Anti-Ace monoclonal antibody reduces Enterococcus faecalis aortic valve infection in a rat infective endocarditis model.Pathogens and disease · 2018Article
- Review
- Efficacy of Telavancin Alone and in Combination with Ampicillin in a Rat Model of Enterococcus faecalis Endocarditis.Antimicrobial agents and chemotherapy · 2017Article
- Article
- Multiple roles for Enterococcus faecalis glycosyltransferases in biofilm-associated antibiotic resistance, cell envelope integrity, and conjugative transfer.Antimicrobial agents and chemotherapy · 2015Article
- Targeting pili in enterococcal pathogenesis.Infection and immunity · 2014Article
- Enterococcus infection biology: lessons from invertebrate host models.Journal of microbiology (Seoul, Korea) · 2014Review
- Article
- Drosophila host model reveals new enterococcus faecalis quorum-sensing associated virulence factors.PloS one · 2013Article
- Enterococcal endocarditis: can we win the war?Current infectious disease reports · 2012Article
- The rise of the Enterococcus: beyond vancomycin resistance.Nature reviews. Microbiology · 2012Review
- Genomic diversification of enterococci in hosts: the role of the mobilome.Frontiers in microbiology · 2012Article
- The Fsr quorum-sensing system of Enterococcus faecalis modulates surface display of the collagen-binding MSCRAMM Ace through regulation of gelE.Journal of bacteriology · 2011Article
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Authors and funding
4 authors.
Funding
Abstract
An Enterococcus faecalis gelE insertion disruption mutant (TX5128), which produces neither gelatinase (GelE) nor the cotranscribed (in the wild type) serine protease (SprE), was found to be attenuated in a rat endocarditis model with a significant decrease in the endocarditis induction rate versus wild-type E. faecalis OG1RF (GelE(+), SprE(+)). TX5266, which has a nonpolar deletion in fsrB and, like TX5128, is phenotypically GelE(-) under usual conditions, was also studied; fsrB is a homologue of agrB of staphylococci and participates in regulation of gelE-sprE expression. Unexpectedly, TX5266 approximated wild-type OG1RF in the endocarditis model and was significantly less attenuated than TX5128. This is in contrast to other models which have found fsr mutants to be as or more attenuated than TX5128. Further study found that the fsrB mutant produced very low levels of gelatinase activity after prolonged incubation in vitro versus no gelatinase activity with TX5128 and did not show the extensive chaining characteristic of TX5128. Reverse transcription-PCR confirmed that gelE was expressed in TX5266 at a very low level versus wild-type OG1RF and was not expressed at all in TX5128. Possible explanations for the increased induction of endocarditis by TX5266 versus TX5128 include the production of low levels of protease(s) or some other effect(s) of the inactivation of the E. faecalis fsr regulator. The equivalent ability of OG1RF and its fsr mutant to initiate endocarditis may explain why we did not find naturally occurring fsr mutants, which account for ca. 35% of E. faecalis isolates, unrepresented in endocarditis versus fecal isolates.
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