Staphylococcus epidermidis
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PROVIDER: PRJNA138643 | ENA |
REPOSITORIES: ENA
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Project description:Background: Staphylococcus epidermidis (SE) has emerged as one of the most important causes of nosocomial infections. The SaeRS two-component signal transduction system (TCS) influences virulence and biofilm formation in Staphylococcus aureus. The deletion of saeR in S. epidermidis results in impaired anaerobic growth and decreased nitrate utilization. However, the regulatory function of SaeRS on biofilm formation and autolysis in S. epidermidis remains unclear. Results: The saeRS genes of SE1457 were deleted by homologous recombination. The saeRS deletion mutant, SE1457DsaeRS, exhibited increased biofilm formation that was disturbed more severely (a 4-fold reduction) by DNase I treatment compared to SE1457 and the complementation strain SE1457saec. Compared to SE1457 and SE1457saec, SE1457DsaeRS showed increased Triton X-100-induced autolysis (approximately 3-fold) and decreased cell viability in planktonic/biofilm states; further, SE1457DsaeRS also released more extracellular DNA (eDNA) in the biofilms. Correlated with the increased autolysis phenotype, the transcription of autolysis-related genes, such as atlE and aae, was increased in SE1457DsaeRS. Whereas the expression of accumulation-associated protein was up-regulated by 1.8-fold in 1457DsaeRS, the expression of an N-acetylglucosaminyl transferase enzyme (encoded by icaA) critical for polysaccharide intercellular adhesion (PIA) synthesis was not affected by the deletion of saeRS. Conclusions: Deletion of saeRS in S. epidermidis resulted in an increase in biofilm-forming ability, which was associated with increased eDNA release and up-regulated Aap expression. The increased eDNA release from SE1457DsaeRS was associated with increased bacterial autolysis and decreased bacterial cell viability in the planktonic/biofilm states. Comparision between SE1457 wild type strain and SA1457 SaeRS mutant strain after 4 hours and 12 hours of growth
2012-01-12 | E-GEOD-29309 | biostudies-arrayexpress
Project description:Background: Staphylococcus epidermidis (SE) has emerged as one of the most important causes of nosocomial infections. The SaeRS two-component signal transduction system (TCS) influences virulence and biofilm formation in Staphylococcus aureus. The deletion of saeR in S. epidermidis results in impaired anaerobic growth and decreased nitrate utilization. However, the regulatory function of SaeRS on biofilm formation and autolysis in S. epidermidis remains unclear. Results: The saeRS genes of SE1457 were deleted by homologous recombination. The saeRS deletion mutant, SE1457DsaeRS, exhibited increased biofilm formation that was disturbed more severely (a 4-fold reduction) by DNase I treatment compared to SE1457 and the complementation strain SE1457saec. Compared to SE1457 and SE1457saec, SE1457DsaeRS showed increased Triton X-100-induced autolysis (approximately 3-fold) and decreased cell viability in planktonic/biofilm states; further, SE1457DsaeRS also released more extracellular DNA (eDNA) in the biofilms. Correlated with the increased autolysis phenotype, the transcription of autolysis-related genes, such as atlE and aae, was increased in SE1457DsaeRS. Whereas the expression of accumulation-associated protein was up-regulated by 1.8-fold in 1457DsaeRS, the expression of an N-acetylglucosaminyl transferase enzyme (encoded by icaA) critical for polysaccharide intercellular adhesion (PIA) synthesis was not affected by the deletion of saeRS. Conclusions: Deletion of saeRS in S. epidermidis resulted in an increase in biofilm-forming ability, which was associated with increased eDNA release and up-regulated Aap expression. The increased eDNA release from SE1457DsaeRS was associated with increased bacterial autolysis and decreased bacterial cell viability in the planktonic/biofilm states.
2012-01-12 | GSE29309 | GEO
Project description:Regulatory role of SrrAB two-component system in Staphylococcus epidermidis growth and biofilm formation
| PRJNA203553 | ENA
Project description:Biofilm formation is considered the most important factor involved in pathogenicity of Staphylococcus epidermidis.We investigated the role of two-component signal transduction system (TCS) srrAB, which was up-regulated under micro-aerobic condition, in the growth and biofilm formation of S. epidermidis.AsrrA-deficient mutant (M-bM-^HM-^FsrrA) derived from S. epidermidis1457 (SE1457), exhibited dramatic reduction in growth and biofilm formation underboth aerobic and micro-aerobic conditions, and more sensitive to several different types of antimicrobial agents, H2O2 and SDS. In New Zealand Rabbit model of S. epidermidis biofilm infection, M-bM-^HM-^FsrrA hardly formed biofilm compared to that of SE1457. Phenotypic alteration was restored to the wide-type levelwhen srrAB were complemented into M-bM-^HM-^FsrrA. Further study found that the initial adherence capacity and production of polysaccharide intercellular adhesion (PIA) in M-bM-^HM-^FsrrA were decreased, while extracellular DNA (eDNA) was increased. Transcriptional Analysisby qRT-PCR demonstrated that expression level of icaRin M-bM-^HM-^FsrrA was up-regulated compared to that of SE1457 under aerobic condition, while down-regulated under micro-aerobic condition;icaA and altE were down-regulated under both conditions. Expression of genes involved in respiratory metabolism, such as qoxB(quinol oxidase polypeptide II), ctaA(heme A synthase), and pfl(pyruvate formatelyase), etc. were down-regulated in M-bM-^HM-^FsrrAunder both conditions. Electrophoretic mobility shift assay (EMSA) revealed that phosphorylated SrrA bound to the promoter regions of icaR, icaA, atlE, qoxB,ctaA, andpflB just like binding its own promoter region srr. Taken together, our results demonstrate that srrAB may provide a mechanistic link between respiratory metabolism, environmental signals, and regulation of biofilm formation in S. epidermidis. Microarrays covering different S. epidermidis genomes were used to assess the impact of the two component system srrAB on growth and biofilm formation, by comparing WT with srrA mutant transcriptomes
2014-11-21 | E-GEOD-47101 | biostudies-arrayexpress
Project description:Biofilm-associated infection by the leading nosocomial pathogen Staphylococcus epidermidis is a major problem for the public health system. Here we used an especially discriminatory, two-step screen to discover key biofilm factors. We identified the transcriptional regulator and SarA paralog SarZ as a novel important determinant of biofilm formation and biofilm-associated infection by S. epidermidis. Notably, a sarZ mutant strain exhibited significantly reduced survival in two different models of biofilm-associated infection. Further, in addition to its significant influence on the transcription of the biosynthetic operon for S. epidermidis biofilm exopolysaccharide, sarZ impacted the expression of a series of virulence factors, including lipases and proteases. As a likely consequence of the regulated proteolytic activity, we observed increased resistance to an important human antimicrobial peptide, indicating a role for sarZ in the regulation of immune evasion. Interestingly, sarZ deficiency led to a hemolytic phenotype, a feature not commonly observed in S. epidermidis. Thus, our study indicates a key role for the SarZ regulator in maintaining the typical S. epidermidis phenotype, which is characterized by pronounced biofilm formation, immune evasion, and suppressed acute virulence, a likely reason for the success of S. epidermidis as a colonizer and pathogen in chronic, biofilm-associated infection. Keywords: Wild type control vs mutant
2008-07-16 | GSE8523 | GEO
Project description:Biofilm-associated infection by the leading nosocomial pathogen Staphylococcus epidermidis is a major problem for the public health system. Here we used an especially discriminatory, two-step screen to discover key biofilm factors. We identified the transcriptional regulator and SarA paralog SarZ as a novel important determinant of biofilm formation and biofilm-associated infection by S. epidermidis. Notably, a sarZ mutant strain exhibited significantly reduced survival in two different models of biofilm-associated infection. Further, in addition to its significant influence on the transcription of the biosynthetic operon for S. epidermidis biofilm exopolysaccharide, sarZ impacted the expression of a series of virulence factors, including lipases and proteases. As a likely consequence of the regulated proteolytic activity, we observed increased resistance to an important human antimicrobial peptide, indicating a role for sarZ in the regulation of immune evasion. Interestingly, sarZ deficiency led to a hemolytic phenotype, a feature not commonly observed in S. epidermidis. Thus, our study indicates a key role for the SarZ regulator in maintaining the typical S. epidermidis phenotype, which is characterized by pronounced biofilm formation, immune evasion, and suppressed acute virulence, a likely reason for the success of S. epidermidis as a colonizer and pathogen in chronic, biofilm-associated infection. Keywords: Wild type control vs mutant Wild type untreated in triplicate is compared to SarZ mutant in triplicate
2010-05-25 | E-GEOD-8523 | biostudies-arrayexpress
Project description:The SaeRS two-component regulatory system of Staphylococcus aureus is known to affect the expression of many genes. The SaeS protein is the histidine kinase responsible for phosphorylation of the response regulator SaeR. In S. aureus Newman, the sae system is constitutively expressed due to a point mutation in saeS, relative to other S. aureus strains, which results in substitution of proline for leucine at amino acid 18. Strain Newman is unable to form a robust biofilm and we report here that the biofilm-deficient phenotype is due to the saeSP allele. Replacement of the Newman saeSP with saeSL, or deletion of saeRS, resulted in a biofilm-proficient phenotype. Newman culture supernatants were observed to inhibit biofilm formation by other S. aureus strains, but did not affect biofilm formation by S. epidermidis. Culture supernatants of Newman saeSL or Newman ΔsaeRS had no significant effect on biofilm formation. The inhibitory factor was inactivated by incubation with proteinase K, but survived heating, indicating that the inhibitory protein is heat-stable. The inhibitory protein was found to affect the attachment step in biofilm formation, but had no effect on preformed biofilms. Replacement of saeSL with saeSP in the biofilm-proficient S. aureus USA300 FPR3757 resulted in the loss of biofilm formation. Culture supernatants of USA300 FPR3757 saeSP, did not inhibit biofilm formation by other staphylococci, suggesting that the inhibitory factor is produced but not secreted in the mutant strain. A number of biochemical methods were utilized to isolate the inhibitory protein. Although a number of candidate proteins were identified, none were found to be the actual inhibitor. In an effort to reduce the number of potential inhibitory genes, RNA-Seq analyses were done with wild-type strain Newman and the saeSL and ΔsaeRS mutants. RNA-Seq results indicated that sae regulates many genes that may affect biofilm formation by Newman.
2015-04-30 | GSE65827 | GEO
Project description:Biofilm formation is considered the most important factor involved in pathogenicity of Staphylococcus epidermidis.We investigated the role of two-component signal transduction system (TCS) srrAB, which was up-regulated under micro-aerobic condition, in the growth and biofilm formation of S. epidermidis.AsrrA-deficient mutant (∆srrA) derived from S. epidermidis1457 (SE1457), exhibited dramatic reduction in growth and biofilm formation underboth aerobic and micro-aerobic conditions, and more sensitive to several different types of antimicrobial agents, H2O2 and SDS. In New Zealand Rabbit model of S. epidermidis biofilm infection, ∆srrA hardly formed biofilm compared to that of SE1457. Phenotypic alteration was restored to the wide-type levelwhen srrAB were complemented into ∆srrA. Further study found that the initial adherence capacity and production of polysaccharide intercellular adhesion (PIA) in ∆srrA were decreased, while extracellular DNA (eDNA) was increased. Transcriptional Analysisby qRT-PCR demonstrated that expression level of icaRin ∆srrA was up-regulated compared to that of SE1457 under aerobic condition, while down-regulated under micro-aerobic condition;icaA and altE were down-regulated under both conditions. Expression of genes involved in respiratory metabolism, such as qoxB(quinol oxidase polypeptide II), ctaA(heme A synthase), and pfl(pyruvate formatelyase), etc. were down-regulated in ∆srrAunder both conditions. Electrophoretic mobility shift assay (EMSA) revealed that phosphorylated SrrA bound to the promoter regions of icaR, icaA, atlE, qoxB,ctaA, andpflB just like binding its own promoter region srr. Taken together, our results demonstrate that srrAB may provide a mechanistic link between respiratory metabolism, environmental signals, and regulation of biofilm formation in S. epidermidis.
2014-11-21 | GSE47101 | GEO
Project description:This study is focused on understanding the molecular basis of protein- and polysaccharide intercellular adhesin (PIA)- mediated biofilm formation by S. epidermidis in PCs. Comparative transcriptomic analysis of S. epidermidis PIA- biofilm positive (AZ22, AZ39) and PIA+ biofilm positive (ST02) strains was performed using a RNAseq approach. Pathway enrichment analysis revealed cellular component GO term (AZ22), two KEGG pathways (AZ39), and two molecular function GO term and 8 KEGG pathways (ST02) were enriched. Remarkably, glutamate biosynthesis and tricarboxylic acid cycle (TCA) genes were upregulated in AZ22 and AZ39, respectively whereas arginine deiminase (ADI) pathway genes were downregulated in ST02. Moreover, genes conferring resistance against antimicrobial peptides (AMPs) and antibiotics such as lysostaphin, fusidic acid and tetracycline were upregulated, thus implying their increased resistance in S. epidermidis grown in PCs. Notably, expression of genes conferring resistance against aminoglycoside (in AZ22) and methicillin (in AZ39 and ST02) were downregulated. This study provided an overview, how biofilm-mediated virulence, antibiotic resistance and metabolic pathways are interlinked and reprogrammed during biofilm maturation in PCs which will be intriguing in development of novel preventive strategies against S. epidermidis transfusion-transmitted infections.
2020-07-14 | GSE154352 | GEO
Project description:Staphylococcus epidermidis is a common causative of nosocomial infections associated with indwelling medical devices. To date, the mechanisms of the pathogenicity and drug resistance of S. epidermidis have not been clearly elucidated. AbfR has been previously identified as an oxidation-sensing regulator that regulates bacterial aggregation and biofilm formation by responding to oxidative stress in S. epidermidis; however, the regulatory pathways of AbfR are underexplored. In this study, we investigated the oxidation-sensing regulatory mechanism of AbfR using TMT10-plex labelling quantitative proteomic and untargeted metabolomic approaches. Integrated analysis of two omics datasets indicated that abfR depletion influenced nucleic acid metabolism and activated the DNA mismatch repair pathway. In addition, several energy-related metabolic pathways, including tricarboxylic acid (TCA) cycle, glycolysis, and arginine metabolism, were remarkably impacted by the deletion of abfR. This study revealed the regulatory networks of the transcription factor AbfR from a multi-omics view and demonstrated that AbfR played a broad role in not only mismatch repair but also energy metabolism, enabling S. epidermidis to constantly sense and adapt to environmental stress.
2020-07-29 | PXD020096 | Pride