Horne D, Hakenbeck R, Tomasz A
J Bacteriol. 1977 Nov;132(2):704-17. doi: 10.1128/jb.132.2.704-717.1977.
Inhibition of peptidoglycan synthesis causes an immediate and massive secretion of both newly synthesized and "old" lipids from several species of bacteria, including streptococci, Staphylococcus epidermidis, and Bacillus subtilis. Lipid secretion occurs in the absence of detectable bacterial lysis. This novel phenomenon was examined in more detail in three strains of streptococci: S. sanguis (group H), S. pyogenes (group A), And S. pneumoniae. The secretion of lipids is specifically induced by inhibitors of peptidoglycan synthesis; it is not caused by inhibitors of protein, ribonucleic acid, or deoxyribonucleic acid synthesis. The occurrence appears to be reversible since penicillin-induced secretion comes to a halt upon the timely addition of penicillinase, correlating with resumption of culture growth. All cellular lipids are secreted in essentially the same proportions as those found in the drug treated bacteria. It is suggested that continued peptidoglycan synthesis may be essential for the integration and retention of lipid material in the plasma membrane.
抑制肽聚糖合成会导致包括链球菌、表皮葡萄球菌和枯草芽孢杆菌在内的几种细菌立即大量分泌新合成的和“旧”的脂质。脂质分泌在未检测到细菌裂解的情况下发生。在三种链球菌菌株中对这一新颖现象进行了更详细的研究:血链球菌(H 组)、化脓性链球菌(A 组)和肺炎链球菌。脂质分泌是由肽聚糖合成抑制剂特异性诱导的;它不是由蛋白质、核糖核酸或脱氧核糖核酸合成抑制剂引起的。这种现象似乎是可逆的,因为青霉素诱导的分泌在及时添加青霉素酶后停止,这与培养物生长的恢复相关。所有细胞脂质的分泌比例与药物处理细菌中的比例基本相同。有人认为,持续的肽聚糖合成对于脂质物质整合并保留在质膜中可能至关重要。