title: Role of the SaeRS two-component regulatory system in Staphylococcus epidermidis autolysis and biofilm formation.
abstract: 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, SE1457ΔsaeRS, 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, SE1457ΔsaeRS showed increased Triton X-100-induced autolysis (approximately 3-fold) and decreased cell viability in planktonic/biofilm states; further, SE1457ΔsaeRS 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 SE1457ΔsaeRS. Whereas the expression of accumulation-associated protein was up-regulated by 1.8-fold in 1457ΔsaeRS, the expression of an N-acetylglucosaminyl transferase enzyme (encoded by icaA) critical for polysaccharide intercellular adhesin (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 SE1457ΔsaeRS was associated with increased bacterial autolysis and decreased bacterial cell viability in the planktonic/biofilm states.
authors.affiliation: Key laboratory of Medical Molecular Virology of Ministry of Education and Ministry of Public Health, Institute of Medical Microbiology and Institutes of Biomedical Sciences, Shanghai Medical College of Fudan University, 138 Yixueyuan Road, Shanghai, 200032, PR China.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Lou
authors.forename: Tao
authors.initials: T
authors.lastname: Zhu
authors.forename: Jian
authors.initials: J
authors.lastname: Hu
authors.forename: Haijing
authors.initials: H
authors.lastname: Ben
authors.forename: Jinsong
authors.initials: J
authors.lastname: Yang
authors.forename: Fangyou
authors.initials: F
authors.lastname: Yu
authors.forename: Jingran
authors.initials: J
authors.lastname: Liu
authors.forename: Yang
authors.initials: Y
authors.lastname: Wu
authors.forename: Adrien
authors.initials: A
authors.lastname: Fischer
authors.forename: Patrice
authors.initials: P
authors.lastname: Francois
authors.forename: Jacques
authors.initials: J
authors.lastname: Schrenzel
authors.forename: Di
authors.initials: D
authors.lastname: Qu
mesh_terms: D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D001433:Bacteriolysis; D018441:Biofilms / Q000254:growth & development*; D004269:DNA, Bacterial / Q000378:metabolism; D017353:Gene Deletion; D015964:Gene Expression Regulation, Bacterial; D005816:Genetic Complementation Test; D050296:Microbial Viability; D015398:Signal Transduction; D013212:Staphylococcus epidermidis / Q000235:genetics / Q000254:growth & development / Q000502:physiology*; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism*
chemical_list: D001426:Bacterial Proteins; D004269:DNA, Bacterial; D014157:Transcription Factors