ArticleNucleic acids research2019
A novel Staphylococcus aureus cis-trans type I toxin-antitoxin module with dual effects on bacteria and host cells.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Membrane selectivity and pore formation of SprA1 and SprA2 hemolytic peptides from Staphylococcus aureus type I toxin-antitoxin systems.The FEBS journal · 2025Article
- Exploring the interactome of the Staphylococcus aureus sRNA Srn_9342 identified a complex formation with RNAIII leading to the modulation of δ-hemolysin expression.BMC microbiology · 2025Article
- Insight into the environmental cues modulating the expression of bacterial toxin-antitoxin systems.FEMS microbiology reviews · 2025Review
- Type I toxin-antitoxin systems in bacteria: from regulation to biological functions.EcoSal Plus · 2024Review
- Small proteins in Gram-positive bacteria.FEMS microbiology reviews · 2023Article
- Mechanism of action ofFrontiers in microbiology · 2023Article
- Thirty Years of sRNA-Mediated Regulation inInternational journal of molecular sciences · 2022Review
- Global transcriptional responses of pneumococcus to human blood components and cerebrospinal fluid.Frontiers in microbiology · 2022Article
- T1TAdb: the database of type I toxin-antitoxin systems.RNA (New York, N.Y.) · 2021Article
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- RNA antitoxin SprF1 binds ribosomes to attenuate translation and promote persister cell formation in Staphylococcus aureus.Nature microbiology · 2021Article
- Diversity and Versatility in Small RNA-Mediated Regulation in Bacterial Pathogens.Frontiers in microbiology · 2021Review
- RNA Regulated Toxin-Antitoxin Systems in Pathogenic Bacteria.Frontiers in cellular and infection microbiology · 2021Review
- A peptide of a type I toxin-antitoxin system inducesProceedings of the National Academy of Sciences of the United States of America · 2020Article
- The Fst/Ldr Family of Type I TA System Toxins: Potential Roles in Stress Response, Metabolism and Pathogenesis.Toxins · 2020Review
- Type I Toxin-Antitoxin Systems in Clostridia.Toxins · 2019Review
- Functionality and cross-regulation of the four SprG/SprF type I toxin-antitoxin systems in Staphylococcus aureus.Nucleic acids research · 2019Article
- Prevalence of Antibiotic and Heavy Metal Resistance Determinants and Virulence-Related Genetic Elements in Plasmids ofFrontiers in microbiology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial type I toxin-antitoxin (TA) systems are widespread, and consist of a stable toxic peptide whose expression is monitored by a labile RNA antitoxin. We characterized Staphylococcus aureus SprA2/SprA2AS module, which shares nucleotide similarities with the SprA1/SprA1AS TA system. We demonstrated that SprA2/SprA2AS encodes a functional type I TA system, with the cis-encoded SprA2AS antitoxin acting in trans to prevent ribosomal loading onto SprA2 RNA. We proved that both TA systems are distinct, with no cross-regulation between the antitoxins in vitro or in vivo. SprA2 expresses PepA2, a toxic peptide which internally triggers bacterial death. Conversely, although PepA2 does not affect bacteria when it is present in the extracellular medium, it is highly toxic to other host cells such as polymorphonuclear neutrophils and erythrocytes. Finally, we showed that SprA2AS expression is lowered during osmotic shock and stringent response, which indicates that the system responds to specific triggers. Therefore, the SprA2/SprA2AS module is not redundant with SprA1/SprA1AS, and its PepA2 peptide exhibits an original dual mode of action against bacteria and host cells. This suggests an altruistic behavior for S. aureus in which clones producing PepA2 in vivo shall die as they induce cytotoxicity, thereby promoting the success of the community.
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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.