ArticleGenes & genomics2023
Phage transcription activator RinA regulates Staphylococcus aureus virulence by governing sarA expression.
Article in Genes & genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- The phage Φ13-encoded transcriptional regulator Ltr controls phage assembly in Staphylococcus aureus.Virology journal · 2026Article
- Anti-Biofilm Properties of Cell-Free Supernatant fromMicroorganisms · 2025Article
- Effect of temperate bacteriophage vB_SauS_S1 on the adaptability and pathogenicity of Staphylococcus aureus ST398.BMC microbiology · 2025Article
- Mechanistic insight ofFrontiers in chemistry · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStaphylococcus aureus is a major human pathogen, that can lead to various community- and hospital-acquired infections. RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism of RinA in the regulation of virulence.
objectiveWe aimed to explore a novel contribution of RinA in the regulation of virulence and provide a new drug target in the treatment of S. aureus infections.
methodsThe specific functions of RinA in S. aureus were analyzed by the methods of growth curve, real-time quantitative PCR (RT-qPCR), subcellular localization, electrophoretic mobility shift assay (EMSA), infection model of Galleria mellonella larvae and the mouse subcutaneous abscess model.
resultsIn this study, we demonstrated that RinA is a protein evenly distributed in the cytoplasm of S. aureus, and its deletion could cause the growth defects. RT-qPCR and EMSA determined that rinA could negatively regulate the expression of sarA by directly binding to its promoter, and vice versa. The Galleria mellonella larvae infection and mouse subcutaneous abscess models revealed that the rinA mutant strain exhibited obvious virulence defects. When sarA is knocked out, the virulence of S.aureus had no significantly changes whether rinA is knocked out or not.
conclusionOur fndings demonstrated that phage transcription activator RinA regulates S. aureus virulence by governing sarA expression.
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