Role of the SaeRS two-component regulatory system in Staphylococcus epidermidis autolysis and biofilm formation
1 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
2 Laboratory of Cellular and Molecular Immunology, Henan University, Jinming Road, Kaifeng, 475004, PR China
3 Department of Orthopedics, The First Affiliated Hospital of Guangxi Medical University, 6 Shuangyong Road, Nanning, 530021, PR China
4 Department of Laboratory Medicine, the First Affiliated Hospital of Wenzhou Medical College, 2 Fuxue Road, Wenzhou, 325000, PR China
5 Genomic Research Laboratory, Service of Infectious Diseases, University of Geneva Hospitals, Rue Gabrielle-Perret-Gentil 4, Geneva, CH-1211, Switzerland
BMC Microbiology 2011, 11:146 doi:10.1186/1471-2180-11-146Published: 24 June 2011
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.
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.
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.