ArticleMolecular microbiology2020
The group A Streptococcus accessory protein RocA: regulatory activity, interacting partners and influence on disease potential.
Article in Molecular microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Molecular characterization of covRS mutations in M1FEBS open bio · 2026Article
- Molecular Characterization of the Group A Streptococcus Virulence-Regulatory System FasBCAX.Molecular microbiology · 2025Article
- Identifying genetic variations ineLife · 2025Article
- Characterization of a novelmBio · 2025Article
- EmergentInfection and immunity · 2024Article
- Identification of distinct impacts of CovS inactivation on the transcriptome of acapsular group A streptococci.mSystems · 2023Article
- Polymeric epitope-based vaccine induces protective immunity against group A Streptococcus.NPJ vaccines · 2023Article
- Hyperphosphorylation of the Group A Streptococcal Control of Virulence Regulator Increases Promoter Occupancy Specifically at Virulence Factor-Encoding Genes.Journal of bacteriology · 2023Article
- Characterization of M-Type-Specific Pilus Expression in Group A Streptococcus.Journal of bacteriology · 2022Article
- The Bacterial Markers of Identification of Invasive CovR/CovS-Inactivated Group AMicrobiology spectrum · 2022Article
- General Phenotype of NADase Induction by CLI Treatment inInternational journal of microbiology · 2022Article
- The CovR regulatory network drives the evolution of Group B Streptococcus virulence.PLoS genetics · 2021Article
- Single Amino Acid Replacements in RocA Disrupt Protein-Protein Interactions To Alter the Molecular Pathogenesis of Group AInfection and immunity · 2020Article
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5 authors at 1 institution in 1 country.
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Abstract
The group A Streptococcus (GAS) causes diseases that range from mild (e.g. pharyngitis) to severely invasive (e.g. necrotizing fasciitis). Strain- and serotype-specific differences influence the ability of isolates to cause individual diseases. At the center of this variability is the CovR/S two-component system and the accessory protein RocA. Through incompletely defined mechanisms, CovR/S and RocA repress the expression of more than a dozen immunomodulatory virulence factors. Alleviation of this repression is selected for during invasive infections, leading to the recovery of covR, covS or rocA mutant strains. Here, we investigated how RocA promotes CovR/S activity, identifying that RocA is a pseudokinase that interacts with CovS. Disruption of CovS kinase or phosphatase activities abolishes RocA function, consistent with RocA acting through the modulation of CovS activity. We also identified, in conflict with a previous study, that the RocA regulon includes the secreted protease-encoding gene speB. Finally, we discovered an inverse correlation between the virulence of wild-type, rocA mutant, covS mutant and covR mutant strains during invasive infection and their fitness in an ex vivo upper respiratory tract model. Our data inform on mechanisms that control GAS disease potential and provide an explanation for observed strain- and serotype-specific variability in RocA function.
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