ArticleMicrobial pathogenesis2008
Role of Mga in group A streptococcal infection at the skin epithelium.
Article in Microbial pathogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 29 citations in OpenAlex.
- Chronic stress unleashes an intratumor phage-fibroblast-B cell circuit to promote tumor growth.Cancer cell · 2026Article
- A Role of Epithelial Cells and Virulence Factors in Biofilm Formation by Streptococcus pyogenesInfection and immunity · 2020Article
- Incremental Contributions of FbaA and Other Impetigo-Associated Surface Proteins to Fitness and Virulence of a Classical Group A Streptococcal Skin Strain.Infection and immunity · 2017Article
- The Regulatory Small RNA MarS Supports Virulence of Streptococcus pyogenes.Scientific reports · 2017Article
- Involvement of signal peptidase I in Streptococcus sanguinis biofilm formation.Microbiology (Reading, England) · 2017Article
- In Vivo Tracking of Streptococcal Infections of Subcutaneous Origin in a Murine Model.Molecular imaging and biology · 2015Article
- Phosphorylation events in the multiple gene regulator of group A Streptococcus significantly influence global gene expression and virulence.Infection and immunity · 2015Article
- A naturally occurring single amino acid replacement in multiple gene regulator of group A Streptococcus significantly increases virulence.The American journal of pathology · 2015Article
- Streptococcus pyogenes biofilms-formation, biology, and clinical relevance.Frontiers in cellular and infection microbiology · 2015Review
- Systematic study of genes influencing cellular chain length in Streptococcus sanguinis.Microbiology (Reading, England) · 2014Article
- Integrated whole-genome sequencing and temporospatial analysis of a continuing Group A Streptococcus epidemic.Emerging microbes & infections · 2013Article
- Vaccination against rheumatic heart disease: a review of current research strategies and challenges.Current infectious disease reports · 2012Article
- Whole-genome association study on tissue tropism phenotypes in group A Streptococcus.Journal of bacteriology · 2011Article
- Dispersal of Group A streptococcal biofilms by the cysteine protease SpeB leads to increased disease severity in a murine model.PloS one · 2011Article
- Loss of the group A Streptococcus regulator Srv decreases biofilm formation in vivo in an otitis media model of infection.Infection and immunity · 2010Article
- Tissue tropisms in group A streptococcal infections.Future microbiology · 2010Review
- Role of the Streptococcus mutans irvA gene in GbpC-independent, dextran-dependent aggregation and biofilm formation.Applied and environmental microbiology · 2009Article
- vfr, a novel locus affecting cysteine protease production in Streptococcus pyogenes.Journal of bacteriology · 2009Article
- Impact of orthologous gene replacement on the circuitry governing pilus gene transcription in streptococci.PloS one · 2008Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Group A streptococci (GAS) primarily cause infection at epithelial tissue sites of its human host. The role of the transcriptional regulator Mga in a humanized mouse model for superficial skin infection was investigated. Inactivation of mga in a skin strain (Alab49) led to loss of virulence. The Deltamga mutant displayed >100-fold decrease in emm (pam) transcript levels, and loss of bacterial-bound plasmin activity. A slight decrease in speB transcription, accompanied by a partial decrease in cysteine protease activity but no change in PrtF2 degradation, was also observed. Mga had no effect on transcription of nra, Nra-regulated pilus genes (cpa, fctA) or other FCT-region genes (msmR, prtF2). Combined with findings on other Alab49 mutants, data show that several essential virulence genes are regulated by Mga or Nra, but not both, implying that any coordinated response during skin infection likely operates at a higher level of transcriptional control. Mga was required for bacterial autoaggregation and biofilm-like growth on an abiotic surface; however, aggregation and biofilm formation have only partial overlap with the skin virulence phenotype. Findings on numerous phenotypes for 7 mutants constructed on the same genetic background yield a detailed, integrated model for GAS pathogenesis at the skin.
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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.