Key laboratory of Medical Molecular Virology of Ministries of Education and Health, Shanghai Medical College of Fudan University, Shanghai, PR China.
BMC Microbiol. 2010 Nov 12;10:287. doi: 10.1186/1471-2180-10-287.
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. 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.
In 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.
The 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.
表皮葡萄球菌已成为最重要的医院获得性病原体之一，主要是因为其能够通过形成生物膜定植于植入的生物材料。大量研究集中在生物膜形成涉及的分子机制上。LytSR 双组分调控系统调节金黄色葡萄球菌的自溶和生物膜形成。然而，LytSR 在表皮葡萄球菌中的作用尚不清楚。
本研究表明，表皮葡萄球菌 lytSR 敲除不改变 Triton X-100 诱导的自溶敏感性。定量肽聚糖水解酶测定表明，表皮葡萄球菌 lytSR 缺失导致细胞外肽聚糖水解酶活性降低，尽管酶谱显示 1457 株和 lytSR 突变株之间肽聚糖水解酶模式没有明显差异。与野生型相比，1457ΔlytSR 产生的生物膜略多，内部死细胞明显减少。微阵列分析显示，lytSR 突变影响 164 个基因的转录（123 个基因上调，41 个基因下调）。具体而言，编码负责蛋白质合成、能量代谢的蛋白质的基因下调，而参与氨基酸和核苷酸合成、氨基酸转运的基因上调。1457ΔlytSR 观察到丙酮酸利用能力受损和精氨酸脱氨酶活性降低，与微阵列数据一致。
初步结果表明，在表皮葡萄球菌中，LytSR 双组分系统调节细胞外肽聚糖水解酶活性、细菌细胞死亡和丙酮酸利用。根据微阵列数据，lytSR 失活似乎会引起严格反应。此外，LytSR 可能通过改变细菌的代谢状态间接增强生物膜形成。
