Abstract
BackgroundStaphylococcus epidermidis has emerged as one of the most important nosocomial pathogens, mainly because of its ability to colonize implanted biomaterials by forming a biofilm. Extensive studies are focused on the molecular mechanisms involved in biofilm formation. The LytSR two-component regulatory system regulates autolysis and biofilm formation in Staphylococcus aureus. However, the role of LytSR played in S. epidermidis remained unknown.ResultsIn the present study, we demonstrated that lytSR knock-out in S. epidermidis did not alter susceptibility to Triton X-100 induced autolysis. Quantitative murein hydrolase assay indicated that disruption of lytSR in S. epidermidis resulted in decreased activities of extracellular murein hydrolases, although zymogram showed no apparent differences in murein hydrolase patterns between S. epidermidis strain 1457 and its lytSR mutant. Compared to the wild-type counterpart, 1457ΔlytSR produced slightly more biofilm, with significantly decreased dead cells inside. Microarray analysis showed that lytSR mutation affected the transcription of 164 genes (123 genes were upregulated and 41 genes were downregulated). Specifically, genes encoding proteins responsible for protein synthesis, energy metabolism were downregulated, while genes involved in amino acid and nucleotide biosynthesis, amino acid transporters were upregulated. Impaired ability to utilize pyruvate and reduced activity of arginine deiminase was observed in 1457ΔlytSR, which is consistent with the microarray data.ConclusionsThe preliminary results suggest that in S. epidermidis LytSR two-component system regulates extracellular murein hydrolase activity, bacterial cell death and pyruvate utilization. Based on the microarray data, it appears that lytSR inactivation induces a stringent response. In addition, LytSR may indirectly enhance biofilm formation by altering the metabolic status of the bacteria.
Highlights
Staphylococcus epidermidis has emerged as one of the most important nosocomial pathogens, mainly because of its ability to colonize implanted biomaterials by forming a biofilm
Among the TCSs identified in the genomes of S. epidermidis, functions of LytSR are unknown, though in S. aureus LytSR has been demonstrated to play a role in bacterial autolysis and biofilm formation
Construction of S. epidermidis 1457ΔlytSR and the complementation strain Because lytSR has been identified as a regulator of autolysis in S. aureus, we hypothesized that lytSR control the rate of autolysis in S. epidermidis, and may be related with biofilm formation
Summary
Staphylococcus epidermidis has emerged as one of the most important nosocomial pathogens, mainly because of its ability to colonize implanted biomaterials by forming a biofilm. The LytSR two-component regulatory system regulates autolysis and biofilm formation in Staphylococcus aureus. Two-component regulatory systems (TCSs) play a pivotal role in bacterial adaptation, survival, and virulence by sensing changes in the external environment and modulating gene expression in response to a variety of stimuli [7,8,9]. Among the TCSs identified in the genomes of S. epidermidis, functions of LytSR are unknown, though in S. aureus LytSR has been demonstrated to play a role in bacterial autolysis and biofilm formation. LytSR two-component regulatory system was firstly identified from the S. aureus genome. Shrama et al reported that a lytS knockout mutant of S. aureus strain UAMS-1 produced more adherent biofilm [11]
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