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.
BMC Microbiol. 2011 Jun 24;11:146. doi: 10.1186/1471-2180-11-146.
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.
表皮葡萄球菌（SE）已成为医院感染的最重要原因之一。SaeRS 双组分信号转导系统（TCS）影响金黄色葡萄球菌的毒力和生物膜形成。表皮葡萄球菌中 saeR 的缺失导致厌氧生长受损和硝酸盐利用减少。然而，SaeRS 对表皮葡萄球菌生物膜形成和自溶的调节功能尚不清楚。
通过同源重组缺失 SE1457 的 saeRS 基因。与 SE1457 和互补菌株 SE1457saec 相比，saeRS 缺失突变体 SE1457ΔsaeRS 的生物膜形成增加，DNase I 处理对其干扰更严重（减少 4 倍）。与 SE1457 和 SE1457saec 相比，SE1457ΔsaeRS 表现出增加的 Triton X-100 诱导的自溶（约 3 倍）和浮游/生物膜状态下的细胞活力降低；此外，SE1457ΔsaeRS 还在生物膜中释放出更多的细胞外 DNA（eDNA）。与增加的自溶表型相关，SE1457ΔsaeRS 中自溶相关基因，如 atlE 和 aae 的转录增加。虽然 1457ΔsaeRS 中积累相关蛋白的表达上调了 1.8 倍，但对多糖细胞间黏附素（PIA）合成至关重要的 N-乙酰氨基葡萄糖基转移酶酶（由 icaA 编码）的表达不受 saeRS 缺失的影响。
表皮葡萄球菌中 saeRS 的缺失导致生物膜形成能力增加，这与 eDNA 释放增加和 aap 表达上调有关。SE1457ΔsaeRS 中 eDNA 释放的增加与浮游/生物膜状态下细菌自溶增加和细菌细胞活力降低有关。
