Molenkamp G C, Veerkamp J H
Antimicrob Agents Chemother. 1976 Nov;10(5):786-94. doi: 10.1128/AAC.10.5.786.
The formation of cell envelope components of Bifidobacterium bifidum subsp. pennsylvanicus was studied by measuring the incorporation of [(3)H]glycine, (14)C-labeled fatty acids, and N-benzoyl-[(14)C]glucosamine into the membrane protein, membrane lipids, and cell wall peptidoglycan, respectively. Inhibition of peptidoglycan synthesis by antibiotics (penicillin G, vancomycin, d-cycloserine, and bacitracin) and by the omission of glucosamine-containing growth factors caused a marked decrease in glycine incorporation into cellular as well as membrane protein, which was accompanied by a considerable enhancement of fatty acid incorporation. The uncoupling of protein and lipid synthesis led to the release of marked amounts of lipids from the cell under these conditions. Arrestment of protein synthesis by antibiotics (chloramphenicol, tetracycline, and actinomycin D) decreased peptidoglycan and lipid synthesis only partially, but did not lead to lipid release. Mg(2+) deficiency of the medium caused about 60% inhibition of growth and lipid synthesis, but protein synthesis and especially peptidoglycan synthesis were much less inhibited. Staphylococcin 1580 arrested the growth and also the synthesis of protein and peptidoglycan. However, the synthesis and turnover of lipids were considerably increased and a release of large amounts of lipids was observed. Peptidoglycan and cellular protein did not show any turnover either during normal growth or after the inhibition of cell wall and protein synthesis.
通过分别测定[(3)H]甘氨酸、14C标记脂肪酸和N-苯甲酰基-[(14)C]葡萄糖胺掺入膜蛋白、膜脂和细胞壁肽聚糖中的量,研究了宾夕法尼亚双歧杆菌亚种细胞壁成分的形成。抗生素(青霉素G、万古霉素、d-环丝氨酸和杆菌肽)以及不含葡萄糖胺生长因子时对肽聚糖合成的抑制,导致甘氨酸掺入细胞蛋白和膜蛋白的量显著减少,同时脂肪酸掺入量大幅增加。在这些条件下,蛋白质和脂质合成的解偶联导致大量脂质从细胞中释放。抗生素(氯霉素、四环素和放线菌素D)对蛋白质合成的抑制仅部分降低了肽聚糖和脂质合成,但未导致脂质释放。培养基中Mg(2+)缺乏导致约60%的生长和脂质合成抑制,但蛋白质合成尤其是肽聚糖合成受抑制程度小得多。葡萄球菌素1580抑制生长以及蛋白质和肽聚糖的合成。然而,脂质的合成和周转显著增加,观察到大量脂质释放。在正常生长期间或细胞壁和蛋白质合成受抑制后,肽聚糖和细胞蛋白均未显示任何周转。