ArticlePLoS pathogens2011
Distinct single amino acid replacements in the control of virulence regulator protein differentially impact streptococcal pathogenesis.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed.
- Molecular characterization of covRS mutations in M1FEBS open bio · 2026Article
- Molecular Characterization of the Group A Streptococcus Virulence-Regulatory System FasBCAX.Molecular microbiology · 2025Article
- EmergentInfection and immunity · 2024Article
- Hyperphosphorylation of the Group A Streptococcal Control of Virulence Regulator Increases Promoter Occupancy Specifically at Virulence Factor-Encoding Genes.Journal of bacteriology · 2023Article
- A Novel CovS Variant Harbored by a Colonization Strain Reduces Streptococcus pyogenes Virulence.Journal of bacteriology · 2023Article
- Characterization of M-Type-Specific Pilus Expression in Group A Streptococcus.Journal of bacteriology · 2022Article
- The Integrative Conjugative Element ICESpyM92 Contributes to Pathogenicity of Emergent Antimicrobial-ResistantInfection and immunity · 2022Article
- CovS inactivation reduces CovR promoter binding at diverse virulence factor encoding genes in group A Streptococcus.PLoS pathogens · 2022Article
- Signaling Peptide SpoV Is Essential forMicroorganisms · 2021Article
- Single Amino Acid Replacements in RocA Disrupt Protein-Protein Interactions To Alter the Molecular Pathogenesis of Group AInfection and immunity · 2020Article
- Polymorphisms in Regulator of Cov Contribute to the Molecular Pathogenesis of Serotype M28 Group A Streptococcus.The American journal of pathology · 2019Article
- Article
- Capsular Polysaccharide of Group AMicrobiology spectrum · 2019Article
- Phosphatase activity of the control of virulence sensor kinase CovS is critical for the pathogenesis of group A streptococcus.PLoS pathogens · 2018Article
- Role of CovR phosphorylation in gene transcription in Streptococcus mutans.Microbiology (Reading, England) · 2018Article
- Identification and Characterization of Serotype-Specific Variation in Group A Streptococcus Pilus Expression.Infection and immunity · 2018Article
- Article
- Use of a Phosphorylation Site Mutant To Identify Distinct Modes of Gene Repression by the Control of Virulence Regulator (CovR) in Streptococcus pyogenes.Journal of bacteriology · 2017Article
- Intergenic Variable-Number Tandem-Repeat Polymorphism Upstream of rocA Alters Toxin Production and Enhances Virulence in Streptococcus pyogenes.Infection and immunity · 2016Article
- Article
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9 authors.
Funding
Abstract
Sequencing of invasive strains of group A streptococci (GAS) has revealed a diverse array of single nucleotide polymorphisms in the gene encoding the control of virulence regulator (CovR) protein. However, there is limited information regarding the molecular mechanisms by which CovR single amino acid replacements impact GAS pathogenesis. The crystal structure of the CovR C-terminal DNA-binding domain was determined to 1.50 Å resolution and revealed a three-stranded β-sheet followed by a winged helix-turn-helix DNA binding motif. Modeling of the CovR protein-DNA complex indicated that CovR single amino acid replacements observed in clinical GAS isolates could directly alter protein-DNA interaction and impact protein structure. Isoallelic GAS strains that varied by a single amino acid replacement in the CovR DNA binding domain had significantly different transcriptomes compared to wild-type and to each other. Similarly, distinct recombinant CovR variants had differential binding affinity for DNA from the promoter regions of several virulence factor-encoding genes. Finally, mice that were challenged with GAS CovR isoallelic strains had significantly different survival times, which correlated with the transcriptome and protein-DNA binding studies. Taken together, these data provide structural and functional insights into the critical and distinct effects of variation in the CovR protein on GAS pathogenesis.
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