ArticleInfection and immunity2014
CcpA is important for growth and virulence of Enterococcus faecium.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Molecular mechanisms of virulence in Enterococcus faecium: integrating Esp, Acm, regulatory RNA networks in multidrug resistant nosocomial infections.Archives of microbiology · 2026Review
- Virulence signature of the endemic vancomycin-resistantMicrobiology spectrum · 2025Article
- Genomic context as well as sequence of bothmBio · 2024Article
- VirulenceFinder forMicrobiology spectrum · 2024Article
- Enterococcal-host interactions in the gastrointestinal tract and beyond.FEMS microbes · 2024Review
- The role of the universal sugar transport system components PtsI (EI) and PtsH (HPr) inFEMS microbes · 2024Article
- The population structure of vancomycin-resistant and -susceptibleMicrobial genomics · 2023Article
- Group B Streptococcus Cas9 variants provide insight into programmable gene repression and CRISPR-Cas transcriptional effects.Communications biology · 2023Article
- Development and Characterization of High-ThroughputFrontiers in cellular and infection microbiology · 2021Article
- Lack of nutritional immunity in diabetic skin infections promotesScience advances · 2020Article
- CRISPR-Cas9-mediated genome editing in vancomycin-resistant Enterococcus faecium.FEMS microbiology letters · 2019Article
- Enterococcal Genetics.Microbiology spectrum · 2019Review
- Transcriptome, Phenotypic, and Virulence Analysis ofFrontiers in cellular and infection microbiology · 2019Article
- CcpA Coordinates Growth/Damage Balance for Streptococcus pyogenes Pathogenesis.Scientific reports · 2018Article
- Article
- Review
- A Multi-Serotype Approach Clarifies the Catabolite Control Protein A Regulon in the Major Human Pathogen Group A Streptococcus.Scientific reports · 2016Article
- Stress Physiology of Lactic Acid Bacteria.Microbiology and molecular biology reviews : MMBR · 2016Review
- The fibronectin-binding protein Fnm contributes to adherence to extracellular matrix components and virulence of Enterococcus faecium.Infection and immunity · 2015Article
- The identification and functional characterization of WxL proteins from Enterococcus faecium reveal surface proteins involved in extracellular matrix interactions.Journal of bacteriology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The collagen adhesin Acm was the first virulence determinant reported to be important for the pathogenesis of Enterococcus faecium in a rat infective endocarditis model. We had previously reported that there was a slight growth delay associated with acm allelic replacement (cat) mutant strain TX6051 used in that study. Recently, we generated a nonpolar markerless acm deletion mutant and did not observe a delay in growth. We therefore performed comparative genome sequence analysis of wild-type strain TX82 and TX6051 and found a single mutation, a nonsense mutation in the ccpA gene of TX6051. After correcting this mutation, the growth defect of TX6051 was abolished, implicating a role for CcpA in the growth of E. faecium. To confirm this, we created a ccpA deletion mutant of TX82, which also exhibited a slight delay in growth. Furthermore, the ccpA deletion mutant was attenuated (P = 0.0024) in a mixed-inoculum (TX82 plus TX82 ΔccpA) rat endocarditis model and also in an in vitro competitive growth assay; a ccpA-complemented strain showed neither reduced growth nor reduced virulence. We also found attenuation in the endocarditis model with the new acm deletion mutant although not as great as that previously observed with TX6051 carrying the ccpA mutation. Taken together, our data confirm the role of Acm in the pathogenesis of endocarditis. We also show that CcpA affects the growth of E. faecium, that an intact ccpA gene is important for full virulence, and that a ccpA mutation was partly responsible for the highly attenuated phenotype of TX6051.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.