ArticleMedical microbiology and immunology2015
Pfs promotes autolysis-dependent release of eDNA and biofilm formation in Staphylococcus aureus.
Article in Medical microbiology and immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 34 citations in OpenAlex.
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- Ways to control harmful biofilms: prevention, inhibition, and eradication.Critical reviews in microbiology · 2021Review
- TatD DNases Contribute to Biofilm Formation and Virulence inFrontiers in microbiology · 2021Article
- Differential Induction of Type I and III Interferons byInfection and immunity · 2020Article
- SpoVG Modulates Cell Aggregation in Staphylococcus aureus by RegulatingApplied and environmental microbiology · 2020Article
- Effect of nicotine on Staphylococcus aureus biofilm formation and virulence factors.Scientific reports · 2019Article
- MgrA Negatively Regulates Biofilm Formation and Detachment by Repressing the Expression ofApplied and environmental microbiology · 2018Article
- Extracellular DNA in natural environments: features, relevance and applications.Applied microbiology and biotechnology · 2018Review
- Interference With Quorum-Sensing Signal Biosynthesis as a Promising Therapeutic Strategy Against Multidrug-Resistant Pathogens.Frontiers in cellular and infection microbiology · 2018Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Staphylococcus aureus is a major biofilm-forming pathogen, and biofilm formation remains an obstacle in the treatment of clinical S. aureus infection. Methylthioadenosine/S-adenosylhomocysteine nucleosidase (Pfs) has been implicated in methylation reactions, polyamine synthesis, vitamin synthesis, and quorum-sensing pathways. In this study, we observed that the deletion of pfs gene in S. aureus NCTC8325 reduced bacterial clumping ability and resulted in the decreased biofilm formation under both static and dynamic flow conditions in an autoinducer-2-independent manner. While the PIA amount was not affected, the pfs mutation significantly decreased the amount of eDNA present in the biofilm and the cell autolysis. Consistent with reduced autolysis, the transcription levels of the autolysin genes, lytM and atlE, were reduced in the absence of Pfs. These data suggest that Pfs promotes autolysis-dependent release of eDNA and biofilm formation in S. aureus, and our findings indicate that Pfs is a potential novel target for anti-biofilm therapy.
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