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Extracellular DNA released by glycine-auxotrophic Staphylococcus epidermidis small colony variant facilitates catheter-related infections
Though a definitive link between small colony variants (SCVs) and implant-related staphylococcal infections has been well-established, the specific underlying mechanism remains an ill-explored field. The present study analyzes the role SCVs play in catheter infection by performing genomic and metabo...
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Published in: | Communications biology 2021-07, Vol.4 (1), p.904-904, Article 904 |
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Main Authors: | , , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Though a definitive link between small colony variants (SCVs) and implant-related staphylococcal infections has been well-established, the specific underlying mechanism remains an ill-explored field. The present study analyzes the role SCVs play in catheter infection by performing genomic and metabolic analyses, as well as analyzing biofilm formation and impacts of glycine on growth and peptidoglycan-linking rate, on a clinically typical
Staphylococcus epidermidis
case harboring stable SCV, normal counterpart (NC) and nonstable SCV. Our findings reveal that
S. epidermidis
stable SCV carries mutations involved in various metabolic processes. Metabolome analyses demonstrate that two biosynthetic pathways are apparently disturbed in SCV. One is glycine biosynthesis, which contributes to remarkable glycine shortage, and supplementation of glycine restores growth and peptidoglycan-linking rate of SCV. The other is overflow of pyruvic acid and acetyl-CoA, leading to excessive acetate. SCV demonstrates higher biofilm-forming ability due to rapid autolysis and subsequent eDNA release. Despite a remarkable decline in cell viability, SCV can facilitate in vitro biofilm formation and in vivo survival of NC when co-infected with its normal counterparts. This work illustrates an intriguing strategy utilized by a glycine-auxotrophic clinical
S. epidermidis
SCV isolate to facilitate biofilm-related infections, and casts a new light on the role of SCV in persistent infections.
Liu et al. investigate the mechanism for small colony variant (SCV) formation in
Staphylococcus epidermidis
and following genomic and metabolomic analysis, implicate a frame-shift mutation in glycine production as a potential cause of SCV formation. The authors also examine the effect of eDNA production and biofilm formation. |
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ISSN: | 2399-3642 2399-3642 |
DOI: | 10.1038/s42003-021-02423-4 |