ArticleJournal of bacteriology2009
Contribution of lipoproteins and lipoprotein processing to endocarditis virulence in Streptococcus sanguinis.
Article in Journal of bacteriology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
44 citing papers in PubMed, 59 citations in OpenAlex.
- A genome-wide in vivo screen reveals fitness pathways required for streptococcal infective endocarditis.PLoS pathogens · 2026Article
- A genome-widebioRxiv : the preprint server for biology · 2026Article
- A novel infective endocarditis virulence factor related to multiple functions for bacterial survival in blood was discovered inbioRxiv : the preprint server for biology · 2024Article
- Contribution of a ZIP-family protein to manganese uptake and infective endocarditis virulence in Streptococcus sanguinis.Molecular microbiology · 2022Article
- Proteoglycan 4 (lubricin) is a highly sialylated glycoprotein associated with cardiac valve damage in animal models of infective endocarditis.Glycobiology · 2021Article
- Time-course analysis of Streptococcus sanguinis after manganese depletion reveals changes in glycolytic and nucleic acid metabolites.Metabolomics : Official journal of the Metabolomic Society · 2021Article
- Genome-wide identification of Streptococcus sanguinis fitness genes in human serum and discovery of potential selective drug targets.Molecular microbiology · 2021Article
- Resistome ofACS infectious diseases · 2020Article
- Intracellular Metal Speciation inACS infectious diseases · 2020Article
- Availability of Zinc Impacts Interactions between Streptococcus sanguinis and Pseudomonas aeruginosa in Coculture.Journal of bacteriology · 2020Article
- Association of NovelFrontiers in microbiology · 2020Article
- Manganese Depletion Leads to Multisystem Changes in the Transcriptome of the Opportunistic PathogenFrontiers in microbiology · 2020Article
- Recognition of specific sialoglycan structures by oral streptococci impacts the severity of endocardial infection.PLoS pathogens · 2019Article
- Gene fitness landscape of group A streptococcus during necrotizing myositis.The Journal of clinical investigation · 2019Article
- Genomic, Phenotypic, and Virulence Analysis ofInfection and immunity · 2019Article
- Streptococcus sanguinis biofilm formation & interaction with oral pathogens.Future microbiology · 2018Review
- Impact of Cell Surface Molecules on Conjugative Transfer of the Integrative and Conjugative Element ICEApplied and environmental microbiology · 2018Article
- Lipoproteins of Gram-Positive Bacteria: Key Players in the Immune Response and Virulence.Microbiology and molecular biology reviews : MMBR · 2016Review
- Involvement of NADH Oxidase in Competition and Endocarditis Virulence in Streptococcus sanguinis.Infection and immunity · 2016Article
- Intrauterine device infection causing concomitant streptococcal toxic shock syndrome and pelvic abscess with Actinomyces odontolyticus bacteraemia.BMJ case reports · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Streptococcus sanguinis is an important cause of infective endocarditis. Previous studies have identified lipoproteins as virulence determinants in other streptococcal species. Using a bioinformatic approach, we identified 52 putative lipoprotein genes in S. sanguinis strain SK36 as well as genes encoding the lipoprotein-processing enzymes prolipoprotein diacylglyceryl transferase (lgt) and signal peptidase II (lspA). We employed a directed signature-tagged mutagenesis approach to systematically disrupt these genes and screen each mutant for the loss of virulence in an animal model of endocarditis. All mutants were viable. In competitive index assays, mutation of a putative phosphate transporter reduced in vivo competitiveness by 14-fold but also reduced in vitro viability by more than 20-fold. Mutations in lgt, lspA, or an uncharacterized lipoprotein gene reduced competitiveness by two- to threefold in the animal model and in broth culture. Mutation of ssaB, encoding a putative metal transporter, produced a similar effect in culture but reduced in vivo competiveness by >1,000-fold. [(3)H]palmitate labeling and Western blot analysis confirmed that the lgt mutant failed to acylate lipoproteins, that the lspA mutant had a general defect in lipoprotein cleavage, and that SsaB was processed differently in both mutants. These results indicate that the loss of a single lipoprotein, SsaB, dramatically reduces endocarditis virulence, whereas the loss of most other lipoproteins or of normal lipoprotein processing has no more than a minor effect on virulence.
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Registered trials
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.